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BIOL 2321_Microbiology for Science Majors - 2321_11_9_23_CH 23
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00:02 Yeah. Um Almost. Ok. . Mhm. So thank you.
00:50 Testing. Testing. Testing. Hey , welcome. We are uh down
01:02 the end here. Uh Let's see week then we have Thanksgiving week and
01:12 day there and then done. so 12345 class periods probably more like
01:22 . Ok. Any case. So any case, uh so we're gonna
01:30 on with unit four. We started Tuesday. Um So obviously none of
01:36 stuff this week is on the Exam starts tomorrow and Saturday. Um
01:43 , there's a weekly quiz, the today uh this week's stuff. So
01:49 your, your, your brain is this stuff. Ok? So just
01:53 until Monday then just do the do quiz on Monday. Ok, after
01:59 Sunday, you know what have Ok. Um I think there's like
02:05 six questions or something like that. uh let's see. Um ok,
02:12 continuing on with 24. So um basically what we're doing here is looking
02:20 um we're coming to in the end , chapter 26. Uh So I
02:26 as well, you know, as if you look ahead at that
02:30 You're gonna go. Oh my There's like a bazillion diseases in chapter
02:35 . Yeah, there's, they cover number of things. I don't cover
02:38 I picked out select once. So, um, and basically it's
02:44 . Here's disease. What causes What are some of the features of
02:50 , of the pathogen? Um What some of the characteristics of the
02:54 stuff like that? Ok. um yeah, I probably not,
03:00 a lot of that. Just, a lot of that material is just
03:03 memorization and stuff, right? Uh 26 material. So, uh any
03:09 , um if you look ahead, know, kind of, I have
03:13 list of what you need to know what to know about each disease.
03:16 just pay attention to that. Uh we're not there yet, we're getting
03:20 . And so right now we're in at the um uh how your body
03:26 disease, basically, right? We on this last time with the innate
03:30 system, uh what you're born with physical chemical barriers. And then um
03:38 begin today, we'll actually start 24 little bit of that today at the
03:43 , uh the adaptive immune system. uh then in the in microbial
03:50 we basically turn it, turn the to the pathogen and what does it
03:57 in terms of overcoming all of these barriers that we have in terms of
04:02 immune system. Ok. And then of diseases is where it kind of
04:06 comes together. Ok. So, , so let's start with this is
04:12 question we had last time. This is the after one. So
04:16 saw this before. Uh, let pull up my picture of the results
04:24 time. Let's see. Ok. . Mm. Looks like looking for
04:43 false answer here. Ok. Only seven people picked the correct answer
04:59 time. OK. Only seven people . Ok. Let's see if there's
05:04 change in that. Yeah, we for a second. Yeah.
05:28 Let's count down here. 98. I paused it one second. So
05:44 most popular answer last time was F . Ok. Let's see what,
05:52 see what you got. Ok. went from 7 to 49 G is
06:00 correct answer? Ok. F stayed 110. That's weird. OK.
06:08 Third line defense. Yeah. B or T cell. That's your adaptive
06:11 system. Its third line defense. . Uh Do you have Clostridium Tetani
06:18 part of your microbiome? I hope . Ok. Um You don't,
06:23 a soil microorganism. Catch it you know, step on a rusty
06:27 . Get a tetanus shot, Um That's where opportunistic pathogens arise.
06:31 from your, what's, what's on and they kind of yet, you
06:36 , uh by accident, typically they in other parts of your body that
06:40 don't normally go to and that's when cause issues, staph infection and stamps
06:44 your skin because membranes, you get puncture wound. Now you, you
06:49 provide a entry point for those OK? Um Yeah, A through
06:54 for all ro OK. So let's at the kind of a summary of
07:00 we did last time. So um remember like 1st, 2nd line
07:05 these double as having secretions as right? Chemical barriers. So um
07:12 so remember that, you know, skin uh mucous membranes and secretions.
07:16 the lining of your body cavities, membranes, OK. Nose throat,
07:22 , etcetera. Um that you you're gonna have various micro environments within
07:28 areas, right? Um The microbes there metabolize, they produce materials that
07:35 affect the ph of the area. oxygen levels can vary. So you
07:40 have um uh a anaerobic and aerobic in various parts of the body.
07:45 it's a but they're very well right? And so this microbial
07:51 right? These guys help keep unwanted out, not all the time,
07:57 you know, they do a pretty job uh As long as your immune
08:00 is relatively healthy. Ok. Uh line defense, remember these are basically
08:06 cell types that come into play uh . We'll talk about these today.
08:12 . Um And then uh in this lymph lymphatic, your lymphatic system.
08:20 so this is what protects against inhaled microbes, lymphatic tissue is heavy in
08:25 cells, T cells or macrophages, cells and they kind of work together
08:31 um things you may inhale things you ingest uh can come into contact with
08:37 cell types in lymphatic tissue, which be very dense in different parts of
08:43 body, armpits, growing tools, different parts of your skin underneath can
08:49 dense areas of lymphatic tissue. And these serve to obviously protect you.
08:56 . Then um this uh this uh uh remember this is kind of the
09:04 this is the point, the uh alarm, right? Warning your body
09:08 maybe an impending infection. Uh Let's something about it. And to remember
09:14 you talk to your cells through chemicals different kinds, right? And so
09:18 immune system, it's cytokines, of various types that have these kinds
09:24 effects to attract cells to the cy infection, to um uh create
09:32 inflammatory response. We'll talk about that , activate different cell types,
09:36 But that's what these to like They can also be internal as
09:42 The uh what we call the um hold on back up here, what
09:48 call the uh not like NLR receptors are internal. So you can like
09:56 viral infection, maybe viral parts bind it and that can trigger a cytokine
10:01 itself. Uh So cytokines is a term for a lot of different chemicals
10:06 in different parts of, of your system. Ok. Um, we
10:11 at different cell types, of Um, some, some the,
10:17 are the py, we'll start with today here in a second P py
10:22 types are one of your primary So, neutrophils, macrophages, dendritic
10:28 do that. Other types are more bliss chemicals as their function like
10:34 Ok. Um, your lymph that's, that's where your third line
10:39 comes in your T cells. B . We'll get into a little bit
10:43 that today. But also NK cells part of that too. Ok.
10:48 they're, they're more, they're more the basket with innate immune system,
10:53 like B and T cells with your adaptive immune system. And
10:57 um, the other thing here is types of pathogens, you gotta deal
11:01 those that are in intercellular virus. learn that bacterial types can do that
11:07 for different purposes. Uh, protozoal can do that. So if you're
11:13 of a cell, you can be from the immune system. So you
11:15 to have a way of finding those out and get rid of them,
11:19 of course, exercise your pathogens do damage while outside of your cells,
11:24 ? So you have to have different to deal with these. OK.
11:27 looked at uh one type natural killer can deal with some types of,
11:32 infected cells. OK. And we'll at some more, uh,
11:37 shortly. OK? And so the main thing that we ended with last
11:42 was this right here, right? self antigens, right? So class
11:48 , class two. So basically your cells, somatic cells is the term
11:53 use for that skin cells, liver , et cetera. Um these are
11:57 contain the class one. So your cells, right? Red blood cells
12:03 their own system. A bo OK. Um And so uh class
12:09 , a very small group, Acro pages, dendritic cells and B
12:14 . And so the types of MH molecules presented to the to the surface
12:20 here, right? Determine what type T cell interacts with it.
12:27 And we'll see the effects of that we move through chapter 24. But
12:33 T cells have specific functions, some them, their role is to get
12:38 of infected cells, right? Like of like a natural killer cell,
12:41 in a different way, right? Other types of T cells bind to
12:48 on a cell with the purpose of to activate that cell type.
12:52 macrophages and cells and B cells become when another type of T cell interacts
12:59 them through these MH C modules. . But it's all about the.
13:03 remember that with these guys here, cells and B cells, it's all
13:10 antigen antigen is what activates it. . So uh for that reason,
13:16 adaptive immune system is a little bit because they have to detect antigen,
13:23 antigen and then in effect results from . OK. So it's gonna
13:27 it's a process. OK. Um right, kind of camp. So
13:34 everything we talked about last time I is any questions about anything is
13:39 OK. All right. So let's at pig cytosis a little more detail
13:45 . So, um I put these up to kind of identify the four
13:50 process here. So uh c for to get cells, uh chemicals that
13:58 attract them to the site of OK. So primarily we're talking about
14:04 , uh macro uh macrophages and dendritic in this function. That's their primary
14:10 is to Vegas. OK. So here, this picture we saw
14:17 So remember these cell types also have these TLR receptors, right? So
14:27 gonna figure ties the cell, but also gonna as a result of the
14:32 here, send out cytokines to attract cells to the area and other
14:38 Um And so the a is for . So we're gonna bind for this
14:44 of pathogen to the uh begay cell , then um ingestion. So a
14:52 zone. So that phag always means feed, right? And so it's
14:57 feeding vesicle if you will, that fuses with a lysosome, which is
15:01 digestive organ that then crunches it up . OK. And so what's
15:08 and that process of crossing it up my words is digestion, right?
15:13 breaking it down. So can uh recycle some of those things uh
15:19 others can get discharged like you see . And so the other thing not
15:23 this diagram is that these cells will MH C molecules. OK. So
15:35 , if this is what it is be a class two. OK.
15:40 so in the process of producing let's say it looks like that and
15:47 will bind with one of these parts the cell or virus, right?
15:55 now it's gonna show that antigen. A G is short for antigen and
16:01 complex will move to the surface. ? And now it can show that
16:09 to the immune system. That's where T cell type would interact with
16:13 OK? And so that T cell will bind OK to this complex and
16:22 the T cell will send out chemicals activate the cell. Um with
16:29 I'm getting way ahead of the game , but to activate a macrophage or
16:34 neutrophil or a dendritic cell, what means is. So if you look
16:39 the arms here, right? Pseudo , right? They got bunches of
16:46 all over, right? And that's when those are dangling out there,
16:51 what can encountering and come in, into contact with an organism, buy
16:57 it, take it in, So contrast with, if the cell
17:02 like this, OK, what we're when we activate it is to turn
17:06 into something like this. Not very picture, but I think you get
17:13 idea, right. So now all pseudopods are popping out, right.
17:18 , now that, that, that's cell here that is activator, it's
17:24 , it's a ploy cell that's now . All these arms now pop out
17:29 enable it to take in stuff. . And so, um that's what
17:33 want them to be like if if you have an infection going on
17:37 that's how they'll best get rid of . OK. So um so with
17:42 binding here you mentioned here, that , yeah, that can vary how
17:51 bound it is. OK. So are certain types pathogens that have a
17:58 , OK? That don't make that they don't bind that well,
18:04 is kind of weak. OK? so cell types like that aren't sis
18:10 easily, right? So that's, that's a virulence factor for the pathogen
18:14 has a capsule. It makes it able to be fois, right?
18:20 we have a way to counteract right? And that's what, that's
18:24 um oh I did have a picture it, Jesus. OK. Hold
18:30 . All right. Let's try again . So where in my drawing?
18:36 there we go. There. You the MH C right here are where
18:41 parts right here, the antigens and binds with MH C and, but
18:47 , then a T cell comes and have some activity. So yeah,
18:50 might jump in ahead of the gun , but we'll see this again in
18:54 24. OK. So, back Opsonin. So this is the defense
18:58 those cells that are kind of slippery can't be easily f OK. So
19:03 have Opsonin think of this as enhanced , or maybe facilitated voc cytosis.
19:12 so what these molecules do is basically the pathogen. OK. So here's
19:18 example of a capsule. So this be uh streptococcus ammonia, which is
19:24 here, but it's thick capsule is halo. You see here,
19:29 So very thick and so it, , it's not easily f at
19:35 But if you produce antibodies to you see here. So antibodies we
19:39 on why shaped structures as A B short for antibody. OK. And
19:45 there's binding sites here as we'll see at that end, two binding sites
19:52 . So too, there's a binding there that we call the FC
19:58 OK. So cells can have a for that, right? Little yellow
20:04 things here. RFC receptors. To bind the FC region can,
20:16 it'll bind that into the, into antibody and the other ends are bound
20:21 the pathogen. And then the whole gets taken in, OK, in
20:26 , right. So now you can a cell type that before wasn't easily
20:32 by using opsonin. And so um as the example in the picture but
20:38 as well, compliment are kind of protein substances floating around in the
20:45 ok, that become active and when become active, one of the things
20:50 do when they become active is to pathogen. And so a cell would
20:57 uh also a compliment receptor. In other words, working very similarly
21:07 to these, it's on the cell , it can bind compliment and complement
21:11 bound to the pathogen and the whole gets taken in, right? So
21:15 are the the two types of right? So this process is called
21:21 . But again, think of it facilitated sycosis is maybe kind of the
21:26 way to think about it. Um OK. Uh Any questions about
21:34 ? Mhm All right. So So there's this other function of macrophages
21:41 dendritic cells. OK. And that just showed that here in this diagram
21:48 there. OK. That's antigen OK? You're showing anti antigen to
21:54 immune system cells that they might not see. OK. And so here
22:02 a T helper cell B into that and it recognizes the MHC class two
22:11 and binds to it and then get of cytokines. OK? And
22:17 this is the example of there's a macrophage, there's an active one.
22:22 you can see all the, basically like a, a rose that blooms
22:28 now, you see all the membranes , you see how the membranes are
22:31 . And these are basically the pseudopods ruffled structure or much of the pseudopods
22:37 out and, and engage in a of phagocytosis. OK. So an
22:43 presentation is a big deal with dendritic cells. That's what you're doing
22:49 your lymphatic system. You're sitting OK? And they will encounter antigen
22:56 it and then t cells that are the area um will, will interact
23:03 it. OK? Um And stimulate , your adaptive system. OK.
23:10 you'll see these things in like I , consoles, armpits growing where you
23:17 these dense collections of lymphatic tissue. see macrophages, indri cells, B
23:22 and T cells all kind of working this way. OK. That's why
23:27 your lymphatic tissues swell. OK. um it's because these things are growing
23:34 growing. So here sore throat tonsils . It's because you have lots of
23:39 immune system cells growing to fight the . OK. Um Any questions about
23:47 ? Hm. So let's look at question. This is gonna take us
23:51 inflammation. OK. Uh So basically looking at which one is going to
23:57 number one, this one happens first everything falls. OK. So that's
24:03 one you wanna pick. This is . So you're gonna pick the one
24:36 happens first because then everything all the ones are gonna follow right after.
24:45 . OK. Cutting down from eight . No good. Yeah, it's
24:59 be cytokine release, right? Number . Number one, number two,
25:06 guest for number two. Which Uh uh yes, it will
25:16 this will be two and that of . Um What's next? Probably see
25:27 then probably, yeah, four would that one then five and then that's
25:36 . OK. So I had to inflammatory response in a couple of
25:44 It's number one is a local right? So we're talking about what
25:50 call the acute ac ute acute inflammatory . Ok. Acute versus chronic.
26:06 . Time time frame, acute 10 days. Ok. Chronic
26:13 months, weeks, months, OK. Um A chronic infection or
26:22 , there's one that gets continually right? Oftentimes there are things like
26:27 basically digestive issues and certain foods cause for people. They can induce inflammation
26:36 your gut uh and then that can . So certain diseases do that
26:42 They can trigger inflammation. Um I , it takes a toll on your
26:47 obviously. And so acute inflammatory response one we've all experienced multiple times
26:56 Um It's meant to be a local . OK. So where the site
27:03 infection occurs, that's where inflammation OK. Uh The goal of information
27:10 to really what that question says. , it's focused on neutrophils,
27:16 It's about getting neutrophils out of your into the surrounding environment to fight the
27:23 because neutrophils are the primary infection fighters this process that then switches to macrophages
27:35 of mop up after them. So, since neutrophils are in your
27:40 , you gotta get them out. so this process of getting them out
27:43 the nucleating blood vessels, ok? um getting them out, right?
27:50 you have to, you have to the cells that make up a blood
27:53 , make it more leaky and they out, but also not just cells
27:58 out, fluid comes out of your too. That, that, that
28:02 into swelling, right? That's where swelling comes, comes from. Um
28:07 , uh but it's all about the of keeping that infection in check right
28:12 in that area. OK. of course, it's gonna involve a
28:16 of these, OK, cytokines of types and, and not even providing
28:25 you all that are involved because it quite complicated. Ok. So just
28:29 pointing out most of the major OK? And so these processes of
28:35 process of getting the cells out of blood is extravasation. OK? Um
28:41 so here's a simple scenario, we introduction of a uh through a wound
28:48 some sort of uh pathogen. Uh in the area, you're gonna have
28:53 like macrophages, um capillaries, of , carrying blood near the skin and
29:00 know, the initial puncture wound in example will damage cells and those damaged
29:06 can really be cytokines. OK? so um that will then um lead
29:15 other cells becoming involved in causing them release chemicals. Ok. So uh
29:22 among them chemo Truss get cells to site of infection. Ok.
29:28 um and so then what happens is of a cascade effect? So one
29:33 these is baso active factors. So is your skin surface, right?
29:39 a blood capillary, you're gonna dilate chemicals, dilate, right? Which
29:45 make bigger, right? Blood vessel bigger and there's two effects of
29:50 ok? And one of those is make the blood vessel bigger.
29:57 So we make it bigger and that's to do what? Slow blood flow
30:05 or increase blood flow. You have garden hose and you put your thumb
30:11 top of it, you get a tight spray on it, right?
30:15 going to increase flow because you're constricting , make it bigger. You're going
30:20 slow it down, ok? You're slow down blood flow in and remember
30:24 is local, it's not happening all your body in the area that this
30:29 is occurring. That's where this will in those capillaries. So I'm gonna
30:35 that. So, um, uh, capillary then dilates, it
30:42 closer to your skin surface and now skin becomes red and splotchy in that
30:48 . Ok? And so, that leads to the redness, it's
30:53 in the area, uh, warm to the touch, of
30:57 Right? And so, um, we slow blood flow down in the
31:03 . OK. Um Remember neutrophils, wanna get those guys out, so
31:07 want to slow it down so you latch on to them and get them
31:10 of the, out of the OK. So we slow blood
31:15 but also we've increased bloodline. So increased bloodline in the area and slowed
31:20 down and that facilitates getting the cells of there. Uh Neutrophils, I
31:26 to um uh fight infection. And so you see one such cell
31:34 in the capillary, OK. And gonna grab onto them. Uh I'm
31:39 show you animation about this but the here you see it, neutrophils are
31:44 pliable. They can give an they can squeeze through like you see
31:51 and get out the other side. ? And now they're out there in
31:56 , in the outside the capillaries and can proceed to biggest of ties cells
32:02 the area. OK. So there's a different set of kinds that
32:06 media in all these things. And so you see a number of
32:10 here, right? Brady Kinon, , prostaglandins, uh et cetera.
32:18 . And so, um this is here, Brady Kinon that helps to
32:24 separate the cells in the blood vessel make an opening for the cells to
32:29 through. OK. They also work other cells to make them uh uh
32:36 chemicals like histamine to work on the vessels too, to intensify the vasodilation
32:42 . Ok. Um, prostate So these things work on nerves,
32:49 endings in the area uh to really the pain, right? Because you
32:54 be aware that you have something going there and a way to do that
32:58 to increase the sensation of pain as result. Ok. That's actually how
33:05 works is to counteract that is to that. So you don't feel the
33:10 . Um, but obviously you want be aware of what's going on.
33:14 . Uh Histamine again is works on vessels. TNF tumor necrosis factor is
33:20 , is a very common one, by many of your immune system cells
33:26 a number of effects, everything from fever in some cases to, to
33:33 uh causing other cells to release various kinds. So it's a very um
33:39 one. I mean, you, , you'll get a blood test and
33:43 look at TNF levels and that will you, are you having an
33:47 inflammatory response of some sort? um so very, very uh
33:52 These other ones c reactive protein in . These are all different types of
33:57 involved in this process. OK. not gonna go into specifics on.
34:02 let's um let's look at animation real and you kind of see the action
34:07 how the um how this works. let's look at, let's look at
34:14 one real quick. This is uh of going back to macrophages. And
34:18 function. OK. So here is macrophage, for example, here's a
34:24 that will be engulfed and there we figure zone forms. Then lysosome fuses
34:34 it. We digest here and then mean c molecule is formed here
34:47 OK. Um In China it up little bit there we go. So
34:54 you see the formation of a MH molecule, right? And that will
35:00 with some of these antigens you see , OK? And then that will
35:09 to the surface and A T for example, can respond to
35:15 OK. So that's the antigen presenting . OK. So let's go back
35:21 here and look at this one inflammatory . There we are. OK.
35:34 . Blow it up. OK? here is our capillary in our right
35:42 this area of the skin. And we'll get a puncture wound.
35:48 OK. Here comes the pathogens and nearby macrophages here in interact,
35:56 So you can get the toll like response, right? Um Like so
36:05 engine, that kind of thing, chemicals, right? These cytokines and
36:12 we go and they'll have their various , vasodilation and then we're gonna close
36:20 here. So these are endothelial cells make up the blood vessel,
36:26 And these things are kind of gonna think of this velcro it's gonna latch
36:32 these neutrophils to slow it down, ? But we've helped helped this by
36:38 blood volume and slowing blood down. makes this an easier process to do
36:44 than other types. Uh Ingrains are kind of, they bind to the
36:50 . And uh so do so do , don't worry about the names
36:54 but this is a way to latch to the neutrophil and slow it
36:58 OK. Then you'll loosen these That's what uh the Brady Ken
37:05 OK. Like so, and then squeeze through. OK. So this
37:13 of, of uh slowing down the is they call margination and this is
37:22 uh diapedesis. You see those terms the the squeezing through of the
37:28 OK. And now they've come out they can begin to figure the
37:32 But obviously, if you're make loosening connections, not only will the cells
37:37 out, but you know, any of fluid will come out as
37:41 OK. Here, the mass cells produce histamine that further it interacts with
37:47 blood vessels. But here you see of the fluid now coming out and
37:51 causes the swelling. OK. um but the healing process is
37:57 So what happens in there is you dead dead cells, both neutrophils that
38:02 died, but obviously, the cells killed and it can form kind of
38:07 layer of, of, of pus some cases. And so you may
38:11 that to complete the healing process. the action of prostate gland is to
38:17 pain. So, uh all part the normal inflammatory response. Ok.
38:24 can, you know, obviously can in severity. You know, if
38:27 have like a splinter in your finger you know, you get a little
38:30 of pain there from inflammation versus something serious. But the same kind of
38:35 are occurring. These of these different cells coming into play, et
38:40 . Ok. Um And then of , it could also repair, could
38:43 involve, you know, a right scab forms part of the healing
38:48 if we're talking about skin damage, . Um Clotting factors may come into
38:54 too to clot blood if there's So all these are of the
38:59 OK? Any questions? OK. with compliment, yeah, these are
39:10 protein factors. OK? They're floating in the blood. Now, if
39:13 look at this, you're gonna see um uh there's about 20 of
39:21 So you guys, if you look it in a book, there's like
39:24 , there's one arrow after another, another, after another uh one activation
39:29 the next activation and so on and forth. OK. And so you
39:35 need to memorize all that stuff. . So, um the ones to
39:42 are C three and C five. . And C three is one that
39:49 uh activated. Uh These are particularly prote proteolysis clea proteins. OK.
39:57 so, uh the C three is into these two parts and the C
40:03 A is what activates the next And so if you look at all
40:06 of these, you'll have multiple of reactions. One activates the next
40:10 the next one, next one cascade . So, um, the,
40:16 are the two major ones here. . C three and C five.
40:20 . When those things are activated, of the effects occur that we're gonna
40:25 about. Ok. So, the, uh, v uh,
40:33 try it again here. So what gonna do then is we're gonna see
40:37 same three effects occur. OK? of how it's activated, right?
40:43 , while in the blood, they're in the inactivated state, we
40:46 to activate them and different processes do . One of them being antibodies,
40:51 probably the major, the major uh . OK? And so um what
40:59 call a classical, so antibodies activate compliments and create the three
41:06 So, ization, inflammation and cytolysis the same three effects no matter how
41:12 activate. OK. In the ultimate , it's really binding. So pick
41:19 bacteria have lots of sugar, protein on the surface. OK? And
41:26 compliment can interact with many of these when it does, it can,
41:31 can become activated. OK. And the last one is called lectin.
41:36 are, are molecules produced in the , OK? That enter the
41:41 And they can also bacteria very commonly uh nanos and similar sugars on their
41:50 . OK? And NANOS in particular one that lectin looks out for,
41:55 . Your cells don't really have OK? But bacterial cells can,
42:00 they can be bound by, by lectin to activate co OK? And
42:07 , uh so again, no matter way you activate it, the outcomes
42:12 the same. OK. So you're have optimization. OK. What you
42:17 about that before active compliment coats the cell takes it in. OK.
42:24 can have uh cytolysis uh where activated um comes together to form a basically
42:33 tunnel in the cell membrane. And that serves to cause license of
42:39 . OK. The um that's what call that in a membrane attack
42:45 OK. Now, gram negatives are susceptible because they have that outer
42:52 right? So these things are built insert themselves in a lipid bilayer.
42:59 ? And of course, the gram has that outer membrane, right?
43:03 positive doesn't they have a thick cell ? So they're not really susceptible to
43:09 particular effect. The gram negatives are . Inflammation. Uh they can assist
43:15 inflammation as well by active active compliment on cells that can cause release of
43:23 cytokines and the inflammatory response. you know it it sort of can
43:27 a combination of these, it doesn't to be just one. but once
43:31 activate, compliment, all these are possible. OK. So um any
43:40 about that, right? So remember itself. Uh these aren't cells,
43:44 are just activated proteins that can produce various effects. Um interferons.
43:55 So, interferons, uh the one of the main functions is anti
44:00 activity. OK. We talked about in the context of, of viral
44:05 against viruses back in chapter six, think. So the type one is
44:09 one we were looking at there. . And so this has the effect
44:14 um a virus infected cell releases this . OK. And so um so
44:23 virus infected cell will likely be killed the process, but it's releasing the
44:31 interferon that can act on other cells the area. OK. So the
44:37 infection itself induces expression of the um . Any cells with a receptor for
44:44 that are in the area will bind that triggers production of transcription factors.
44:49 talk about that in chapter 10. . And so that means the expression
44:53 antiviral proteins that can either either uh degrade the viral genome or, and
45:00 interfere with translation of it. Um that case, the cells protected.
45:06 any any non infected cells can potentially protected by this type one interferon.
45:14 . Um And so the type one your firm was one of the first
45:19 products to be mass produced um using genetic engineering techniques. And with the
45:28 that, you know, it's any activity would be, you know,
45:30 be great and we could put it the pill or whatever market, it
45:35 lots of money or didn't work out well. It's, it's effective in
45:40 , you know, those who have a bad viral infection can get the
45:45 of interference in the hospital. And it can be effective in that
45:49 , but not as like a widespread that you would take as a pill
45:53 because it turns out to be kind toxic and high doses, it doesn't
45:57 a good long shelf life. Uh there's certain restrictions on it, but
46:01 know, in certain scenarios like uh as a as a shot uh
46:07 to counteract an infection, it is , but um not in a
46:12 Uh it was, it was hopefully to be where you can make lots
46:16 money selling pills and stuff in your , just didn't work out. But
46:19 , um uh if you're hospitalized with viral infection, you might get a
46:24 of this uh to help. And the type two is one
46:29 you know, we talked about activating fake acidic cell type, right?
46:32 more of those pseudopods, right? so that's kind of uh what it
46:36 do. It can also increase MH antigens, right? So if you're
46:40 this, if you're doing that, , you're causing it to make more
46:45 these MH C molecules, right? make more of these and made C
46:52 , for example. And if you're that, then you're increasing the potential
46:56 them to bring engine to the right? So now these can travel
47:04 show antigens. So if you're telling cell make more of them, then
47:09 cell will do more of that. then now that, that will enable
47:12 to detect, you know, antigens may be in your body and do
47:17 about it, right? So that's of what that, what that effect
47:20 . Ok. Um Any questions about if you OK. So fever,
47:30 think this is the last one of innate immune system. Uh So fever
47:35 all about manipulating the body's thermostat. . So the hypothalamus which is,
47:44 course, uh your brain, It will, you know, you
47:49 a core body temp you maintain 37 plus or minus half a degree
47:54 Um And uh there are substances like , it says pyrogens, right?
47:59 name pyro means fire, right? , creating fire in the body.
48:03 so you can have uh what are exogenous pyrogens which are uh bacteria,
48:09 types, viruses uh can cause this others. And so when they're in
48:14 body, they actually trigger endogenous right? And so things like tuber
48:21 factor, for example, interlooping one another one. And so what they
48:27 when active is to go to the , basically crank thermostat up.
48:34 So here's a basic scenario here. we have a regular set point.
48:39 is what you're tuned to most of time. Ok. And pyrogens can
48:46 that. Ok. So much uh, we had this cold
48:51 what week or two ago, that you're cold, you know,
48:56 go inside the house. My dorm cranked the heat up. Right.
49:01 didn't, in your room didn't instantaneously to the 78 degrees or whatever you
49:07 . Right. You have to, still felt cold until that room warmed
49:12 enough, right? So you have catch up to it. And so
49:16 , once, when your thermostat and body is cranked up, you're gonna
49:21 cold until you get there right? you, until you, until uh
49:25 , your body, uh until you that temperature of the new set
49:30 OK, you're gonna feel chilly and all experienced this, right? And
49:35 when you're finally at that new high , you're not really wanting to do
49:42 . All right, because you don't that well. But even though you've
49:45 that temperature, uh but it is a function by being at this elevated
49:51 for a while. Ok. um typically what happens is you kind
49:56 oscillate back and forth. So remember , if you're at, if you're
50:00 the new set point now and it a little bit, you're gonna feel
50:05 until you catch up with that new set point, do you typically go
50:09 up and down? Because you feel , chills, hot chills. And
50:14 until finally you've overcome the infection, is, represents the ebb and flow
50:20 these pyrogens as you're fighting the Ok. And so uh once the
50:26 breaks, we call it, then get back finally to your regular set
50:36 body. Well, pathogens um like bacteria in your body. Um they
50:44 at 37 ft right, 98.6 Um And so, if you elevate
50:52 , it's gonna slow the growth OK? As well. It lowers
50:58 of iron. Ok. So it out uh iron, of course,
51:03 a vital nutrient. OK. Iron a lot in a lot of enzymes
51:08 in these redox reactions we've learned And so it's a vital component to
51:15 growth. Ok. So we hold to it, of course,
51:18 we have a hemoglobin in our red cells, right to bind oxygen,
51:22 we have a bunch of other molecules well, right? Because it's important
51:25 us obviously too. So if we get, keep it away from it
51:30 too slows their growth. OK? elevated temp seems to do that.
51:36 . Um Of course, they also chemicals that they release that buy an
51:41 . So it's like we're fighting a of war there. But um but
51:45 increases t selective, right? So cells as we'll learn, um one
51:51 of them really controls the whole adaptive response. And so when you're,
51:57 you're increasing their overall activity, then really mobilizing your adaptive immune system.
52:03 ? So the other thing this does by slowing growth down, but through
52:08 temp, keeping iron away, um buys us time. So time,
52:14 using time is a, is a of both what we do and what
52:20 pathogen does. So, think of , a pattern can, can,
52:26 increase time by hiding out from the system, right? So being inside
52:30 a cell hidden from the immune system a way to for it to buy
52:34 , right? Um it can do things to hide from the immune
52:38 And so if it's hidden, it grow, right? We know how
52:42 bacteria can grow, right? So give them time before they become found
52:49 . By that time, they may proliferated quite substantially. OK? But
52:53 the other hand, if you slow down, that buys you time because
52:59 your adaptive immune system doesn't work right? It's gotta detect androgen,
53:06 to it and create an effect and takes time. So this is one
53:10 for your body to buy time to their growth down. You can find
53:14 out, produce immune response. So time, time and it works
53:20 both sides here. OK. Um . Any super elevated temperature like 100
53:33 four for several hours, that's not either. So there is a
53:39 right? But within reason fever does helps you. Ok. So let's
53:45 kind of recaps the stuff we, , we talk about, uh,
53:53 . So let's see here. looking for the true correct answer
53:58 That's true. Mhm. Ok. , uh, count down from
54:51 uh, 82. Ok. Let's here. Yeah. None, none
55:00 these are right. Ok. pyrogens induced fever. Remember the attack
55:06 ? That's a compliment that does, , um, doesn't involve MHC
55:11 If you're on type one, that's opsonin facilitate trig csis complement is in
55:18 cells of protein. OK. Um right. So let's uh uh
55:29 So any questions before we move on 25 a little bit to get into
55:33 little bit of antibody or, or immune system? OK. Um
55:43 So third line defense is where we're . OK. Um to sing first
55:52 engines in general and then B cells T cells. OK. So looking
55:59 at the system, OK. kind of division of labor here.
56:04 one half is about uh dealing with pathogens. The other half intracellular
56:13 OK. So human immunity is B . So immediate immunity T cells.
56:20 . So your B cell types when active when uh in response to
56:27 Remember this is what controls the whole here. All of it is presence
56:31 an OK. So your plasma cells form the antibodies but you also form
56:37 the same time. Memory cells So you got memory to your adaptive
56:43 system um based on having been stimulated some point through an infection or through
56:59 . Remember an an an antibody can't inside of a cell and bind to
57:05 virus, let's say right? It does their work outside the cell.
57:09 . So, hence extracellular car, . Uh T cell types um and
57:18 into cytotoxic T cells. OK. these guys kind of kind of but
57:24 in the same way similar to any killer cells looking for infected cells.
57:32 Remember natural killer cells look for changes the inmate c molecules on the
57:37 This looks for cells presenting antigen to . OK? And the other types
57:44 T cells are called helper cells to ourselves. And there's two types,
57:49 type uh and both I should say of these the cytotoxic T cells,
57:55 helper cells, they do their work on the types of MH C molecules
58:01 recognize, right. So cytotoxic T , mh C ones. So remember
58:06 these are, right? Your body , skin cells, liver cells,
58:10 , et cetera, right? So of those cells in your body gets
58:14 , potentially these can find them out deal with them. OK. So
58:21 your inmates see two types B dendritic cells, macrophages. So uh
58:27 type ones, this is what interacts those macrophages. Dendritic cells. B
58:33 interact with T helper type two, ? So, it's gonna be a
58:36 of labor with these different types of cells. OK. And so um
58:42 so it does for many B it requires this interaction, then activate
58:52 to do to do that. They plasma cells and memory B cells,
58:57 requires the help of a of A cell with them to get them to
59:01 that. OK. Um And so , in terms of, you
59:07 plasma cells hang around your body once made for maybe two months and then
59:14 kind of go away. OK. cells last for decades. OK.
59:20 3040 years. OK. Um You have to kind of spruce them up
59:28 you will by getting a booster OK. Every 10 years or
59:33 like for tennis, I think it's 10 years. So that because they
59:37 kind of over time kind of dwindle in terms of their effectiveness, the
59:41 of antibodies they produce. Uh, you kinda have to give him a
59:46 every now and again. OK. OK. So that's a good question
59:53 . It has to do with antibody . OK? I mean, not
60:02 . Your best shot. So And OK, let's count down from
61:03 . Bye. Let's see. Uh read it for myself here. A
61:12 true. Oops A is true. That's true. That's true. Uh
61:25 mean, if that's true, that's . They're all true. Yeah.
61:32 . All right. So we'll go these here. OK? Um So
61:39 and foremost B cell types B T cells, it's all about
61:44 OK? So the, and the epitope thing is really just scope,
61:50 engine is a bigger entity. And the engine you have a specific binding
61:55 that's the epitope. OK? So epitope you see here, colored in
62:01 , right? So the, the entity, the whole thing, it's
62:06 engine but it binds specifically an area the engine, what we call the
62:13 . OK. And so what's an ? Well, it can be lots
62:17 things, right? It can be we're talking about pathogens, it can
62:20 , you know, outer membrane molecules the outer membrane of a gram negative
62:26 uh molecules on the popping out of you know, of a grand pos
62:31 could be a flagellum for feri it be a capsule, it could be
62:37 uh a pylas, it could be , you know, the proteins that
62:42 out of a virus, right? be any of those things. Um
62:45 could be pollen, mold spores, ? These are things we're allergic
62:48 those are antigens your your cells are to. Ok. So um generally
62:56 can have um again, it goes to binding, right? Tight
63:02 makes good antibodies. OK. And um protein engines tend to be the
63:11 the ones that produced, the more response in terms of antibodies. So
63:16 call immunogenicity is kind of your ability form an immune response. And proteins
63:24 do that the best because there's lots variety of proteins and protein sequences can
63:29 in different shapes. And these are features that enhance the immune response.
63:35 , certainly sugars, carbohydrates can be antigen. Uh but there, there's
63:40 the, the same variety of forms carbohydrates or fats that proteins have.
63:46 so it's proteins one typically than sugars . Pretty way below. And then
63:55 are nucleic acids can be an but uh we'll learn next week with
64:02 that aren't so good. Um as A as an antigen like for
64:07 right? A vaccine against the That was what the meningitis vaccine is
64:11 you got is, is was used the capsule, right? With the
64:17 , which is carbohydrate, but we enhance it by adding a protein to
64:22 . And so, so we call conjugated vaccine. We're conjugating the sugar
64:26 the protein because that makes it a produces a better immune response.
64:32 So there's things you can do like . OK. So my mind here
64:36 protein engines tend to give the best . OK. So um so just
64:43 at basic structure of antibody, I drew A Y which is kind
64:48 uh simplistic, but we have to a little bit more to it,
64:51 ? We have uh there's actually two here. OK. Anyway, we
64:57 see it over here. So you a variable that the V OK.
65:00 so this is all protein rightly peptide , right? So the minimize sequences
65:06 in their variable sections. OK. that's where the engine binding occurs.
65:13 . And it's gonna be through an within the larger. OK. So
65:21 have two binding sites per antibody. . And we have a region
65:27 The C stands for constant. So it has the same the mio
65:34 a sequence in those sea regions. . And so the antibody classes.
65:42 IG is short for immunoglobins of And we call these isotype,
65:52 That's on our next slide. We them isotype A GVM uh A GDE
66:00 . OK. And um the other is as we saw before is that
66:06 portion, right? That's what this that combined. This can be a
66:14 , for example, OK. uh dendritic cell, right? These
66:22 all um big acidic types and they have these f circles on the
66:30 And that's how they, this is optimization thing. OK. Um So
66:35 we look at the different isotype, do we define that? How do
66:39 define an isotype? Well, if have um uh here are three
66:46 two IGAS and an IgG. So we identify uh the IGAS from
66:55 IgG by the sequence in that constant . OK. So they differ in
67:04 A, all IGAS will have the amino acid sequence in the constant
67:10 All IgGs will have their own specific . OK. It's how you can
67:16 one from the other A, from G from A, the what have
67:21 . OK. So that's what we isotype. OK. So in
67:26 OK. Within an IG A um sorry, uh they possess the um
67:39 differ in the uh um and binding , of course. OK. So
67:48 can have an IG A that responds X an engine here and this one
67:55 to a different one. OK? just generically calling these things and this
68:01 antigen X. This one can respond antigen Y. OK. Just means
68:07 they can respond to different ans, ? You can have, you have
68:09 bunch of igas that respond to and and you can have a bunch that
68:15 to what? Right. So just they vary that way because you can
68:19 that variable region. OK? Um isotype and idiotype, right? So
68:27 looking at different different molecules of the isotype that bind different engines within that
68:35 . Those are different idiotype. So idiotype. This a idiotype that
68:42 Is that makes sense. Yeah. again, within an isotype class,
68:47 have different idiotype because those antibodies can to different antigens. OK? Um
68:56 what kind of effect do you get binding and antibody? Well, one
69:01 the main ones is this. So that uh everybody says each one has
69:07 binding sites, you can kind of cells together. OK? And that's
69:13 glutin nation. OK? And so you're doing is you, you have
69:23 two infectious units, right? By them, you're reducing the number,
69:29 when we see these types that can the what's called the PTER form?
69:39 , right? IgM can do OK. So you see you have
69:49 , 10 binding sites. So you have 10 individual pathogens in the
70:00 right? And now we can bind all up. So you've taken them
70:06 the individual units to um one because bound them all up by this 10
70:17 monster, so to speak, That's what IgM can do.
70:21 So I mean optimization, we saw before. OK. So we're familiar
70:26 that. The other feature is um antibodies. OK. Um So that's
70:35 a feature of um IG A and the COVID vaccine promoted to pathogens like
70:50 stick to your uh mucus mucus membranes your lungs, uh trachea, et
70:57 . Uh So if you can keep from adhering, uh then you basically
71:02 it, they can't stick and get of them uh toxins as well.
71:06 remember that two can be bound by . That's a tetanus vaccine works that
71:18 . OK. Then uh activating compliment talked about that before. And then
71:23 one here is, so we talked it in the context of eosinophils.
71:30 right there dealing with large passages, . That's a collective effort.
71:37 You can't focus at times this thing one cell. It won't happen.
71:44 too big, right. So you attract cells to the site,
71:50 That can release toxins, chemicals to it. And the way to do
71:54 is to attract them through, have buy into antibodies that are bound to
72:02 pathogen. So that antibodies bind, make antibodies to the pathogen, that
72:07 cells can bind to those antibodies and they sit there and then they can
72:11 their chemicals. And so you see release of these because you have so
72:16 of the, of your, of cells, they are stuck to
72:20 They all the chemicals and that collectively kill the pathogen. And this can
72:24 something like these literally can be a . How am I, how he
72:30 have a worm in my body? , they're tiny but you, you
72:34 , you know, different types of parasites and, and, um,
72:39 you know, and you get them puncture wounds. They, in
72:50 but, uh, you know, not as common in most parts of
72:53 world as others, but you you can certainly get these things.
72:59 , if, uh, if you livestock, you know, you worm
73:03 animals, right, cows, uh, to protect against things like
73:07 . Ok. But you know, you can get those as gross as
73:11 may seem. Um Anyway, so the name for this, it's a
73:15 of syllables there, right? So always use a DC C but antibody
73:21 , you can see that right? are part of it, cell
73:24 So you bring different cells, the and then cytotoxicity killing, killing the
73:30 . OK. Um I think that it for today. Uh Let's take
73:37 look. Yes, stop, OK. Yeah. Uh please.
73:48 . See you. Uh Hi So this is from the unit
73:56 And so this question, I was little bit confused about as to why
74:00 not transcriptional control. OK. So . So this is where we're having
74:07 try the fan. OK. So the trip opera and we're gonna
74:15 of course, the RN A, ? And then we're gonna form the
74:19 enzymes. And so the pathway that tryptophan, right? OK. So
74:25 we've made it so this can so this is uh this enzyme one
74:31 , this enzyme two and so So this can actually interact with the
74:37 here. And in doing so you're blocking and making any more tryptophan because
74:44 inhibiting this enzyme. And so so that's what we're doing here.
74:48 so if you're doing that, you're dealing, you're manipulating a protein here
74:54 , to affect expression. That's why post translation because from my understanding,
74:58 thought it was part one I thought was,
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