2) Avoiding Phagocytosis

in this video, we're going to talk about how some pathogens have evolved mechanisms of avoiding fake ghosts Itto sis in order to avoid the immune system. And so first we need to recall from some of our previous lesson videos that we discuss the process of fabio psychosis in detail. And so recall from those older videos that fake acidic cells are able to destroy microbes in a series of steps that involves chemo taxes, recognition, attachment, engulf, mint infusion. And so if you don't remember these steps of photosynthesis, be sure to go check out those videos before you continue here. Now that being said, some pathogens once again have evolved mechanisms of avoiding an encounter with fabio sites and so certain pathogens can avoid encountering fake acidic cells by using one of two mechanisms that we have numbered down below one and two. And so the first mechanism of avoiding an encounter with a ghost sites is through the production of the enzyme called C five A. Pep. Today's peptide aces are enzymes because they end in a sec that are going to break peptide bonds or break down proteins. And so C five A. PEP today's is an enzyme that breaks down the protein C five A. So it degrades the complement system protein C five A. And you might recall from some of our previous lesson videos when we discuss the complement system that C5 A is a complement system protein that serves as a chemo attractant in order to recruit fag acidic cells to the site of infection. And so by breaking down the protein C5 a Fag ascetic cells will not be recruited to the site of infection and that can allow a pathogen to avoid an encounter with the fake ghost site. And so if we take a look at our image down below on the left hand side, you can see how C. Five A. Pep today's can degrade C five A. And so notice that this blue microbe over here on the left hand side is producing an enzyme called C. Five A. Pep. Today's and C. Five A. Pep. Today's which is produced by this pathogen can degrade the protein C. Five A. And so notice that we have degraded C. Five A. And so by degrading C five A. There will be no C five A. To serve as a chemo attracted to recruit the Fargo civic cell. And so because there's no recruitment of the Fargo civic cell, the fatigue, acidic sell the I'm sorry the pathogen can avoid an encounter with the specific cell. And so notice that this macrophage over here saying hmm, where did that microbe go because they're not able to be attracted to the site of infection. So that's one way to avoid an encounter with the famous site. Now the second way is through the production of membrane damaging toxins. And so membrane damaging toxins as their name implies are going to be toxins that cause damage to the membrane. And so they can kill fabio sites and other cells as well. And so they can actually form pores or holes in the membranes of fake ascetic cells and cause those fake ascetic cells to lice or rupture. And so notice that in our image, down below on the right hand side, we're showing you how some pathogens can produce membrane damaging toxins to avoid an encounter with a fake news site. And so notice that here we have a micro a pathogen and this pathogen is producing and releasing these little pink molecules that are membrane damaging toxins. And the membrane damaging toxins can again cause damage to the membrane of the fake acidic cell create pores or holes in the membrane of the fake acidic cell. And that can also ultimately lead to the license or LISZT fake acidic sell a LISZT macrophage for example. And so of course this is going to allow the pathogen to avoid an encounter with the macrophage. Now, it is also important to note that some pathogens have evolved the ability to survive to go psychosis by faith specific cells and induced apoptosis once they're inside the cell. So it could be a process similar to this except the pathogen would actually be engulfed and once the pathogen is engulfed, it would then cause the uh the fact ascetic cell to undergo apoptosis. And so this here concludes our brief lesson on how some pathogens have the ability to avoiding an encounter with fabio sites. And as we move forward, we'll talk about other methods of avoiding Figo psychosis, so we'll get to talk about those other methods as we move forward, so I'll see you all in our next video.

Why do some pathogens destroy the host organism's C5a proteins?

• A. The phagocytic immune cells are not attracted to the pathogen without C5a.
• B. The phagocytic immune cells cannot bind to the pathogen without C5a.
• C. The membrane of the phagocytic immune cells degrades without C5a.

What benefit do pathogenic bacteria obtain from secreting membrane-damaging toxins?

• A. The toxins will damage any surrounding immune cells.
• B. The toxins will stop the immune cells from phagocytosing the pathogen.
• C. The toxins will stop the immune cells from sending messages to other immune cells.
• D. All of the above.
• E. None of the above.

in this video, we're going to continue to talk about how some pathogens can avoid fagot acidosis by talking specifically about how some pathogens can use capsules and M proteins to avoid optimization. And so first we need to recall from some of our previous lesson videos what the term optimization means. And so recall that optimization refers to the process that makes microbes easier to bind or engulf during Figo psychosis. And so once again some pathogens can prevent optimization and so by preventing optimization they make fargo psychosis more difficult and therefore they can avoid fargo psychosis. And so some pathogens are able to prevent optimization by the production of a capsule. And so recall from some of our previous lesson videos that some bacteria have a bacterial capsule which is an outer layer that surrounds the cell and consists of carbohydrates and proteins in some cases. And so these capsules, they can prevent immune cells and obstinance, like the complement protein C3B, from adhering to the pathogen. And so by preventing immune cells and obstinance from adhering to the pathogen. That will avoid optimization and again avoid fabio psychosis. Now very similar to capsules. The production of the cell wall protein called the M. Protein. You can also allow a pathogen to avoid optimization. And so what happens is the M protein will bind to another regulatory protein or inhibitory protein that is going to be degrading the enzyme C. Three convert taste, which is important for complement system activation. And so by Degrading C. three converted, thereby that is going to inhibit or block the production of uh C. Three B. The complement protein C three B, which again we know acts like an option in. And so if we take a look at our image down below, we'll be able to get a better understanding of this idea. So notice on the left hand side, we're showing you how capsules can block C. Three B binding. And so notice that we have to microbes, we have this microbe on the left that is in blue and then we have the microbe that's on the right. And notice that the microbe that is on the left does not have a capsule. And because it does not have a capsule, the option in protein C3B is capable of binding to the surface of that microbe and therefore obscene ization will take place and that means that this microbe is likely to be engulfed through the process of photosynthesis. However, the microbe on the right notice has a bacterial capsule which is this outer layer that's represented in yellow. And that outer layer again consists of carbohydrates and proteins. And so this outer capsule can block the binding of C. Three B. So C three B cannot bind. And if C3B cannot bind, what that means is that there is no optimization. And so by preventing optimization with the capsule that is going to allow it to avoid fagot acidosis. Now on the right hand side, we're showing you how the M protein can block C. Three convert ease. And so what you'll notice is that the cell over here on the left is producing this M. Protein on its cell wall. And so this M protein will associate with an inhibitory protein, this little purple structure or regulatory protein And the inhibitory protein will basically Degrade C3 converts. And you might recall when we covered the complement system in some of our previous lesson videos that C3 convert taste is an enzyme that is important for complement system activation. And so by um Degrading C3 convert C3 converts. This is going to be blocked and it will be blocked from making the option in C. Three B from C three. So usually what happens is C three convert taste will be involved with converting C. Three into C. Three A. And C. Three B. And then C three B. Would serve as an option in However, if there is M protein that means it will associate with the inhibitory protein, the inhibitory protein block C three converted. And then what that means is C three will not be converted into C. Three B. And so by blocking C three convert taste, it is blocking the production of an option on. And that is going to avoid optimization and that will avoid fabio psychosis. And so this year concludes our brief lesson on how pathogens can use capsules and M proteins to avoid optimization and therefore avoid fabio psychosis and we'll be able to get some practice applying these concepts and learn more as we move forward. So I'll see you all in our next video.

The C3b complement protein is incredibly important for opsonization of pathogenic material. How do some pathogens avoid opsonization by interfering with C3b?

• A. Pathogen has outer layer that C3b cannot bind to.
• B. Pathogen inhibits the functions of C3 convertase.
• C. Pathogen stops the formation of C3b.
• D. All of the above.

in this video we're going to talk about how some pathogens can use the fc antibody receptors to prevent optimization and therefore avoid Figo psychosis. So first we need to recall from some of our previous lesson videos, the typical structure of an antibody is a Y shaped just like what you see down below and within this typical structure of the antibody. We have the F. A. B regions which are going to be the antigen binding regions and then we also have the Fc region which is like the stem of the Y. And so recall from our previous lesson videos that when antibodies do bind to a pathogen it is going to be the FC region that is going to be pointing outwards and can serve as an option in for fabio sites and the F A B region is going to be pointing inwards towards the pathogen, as you can see down below on the left hand side and so in the left hand side of our image, notice that we're showing you microbes that do not have FC receptors. Microbes without FC receptors will allow the antibodies to bind normally with their uh antigen binding regions binding to the pathogen and they're fC regions pointing outwards away from the pathogen that will allow for fabio sized hostess to occur normally. However, again, some pathogens have fC receptors, FC antibody receptors and these are surface proteins that will bind to the fC regions of antibodies and by binding to the fC regions of antibodies it can interfere with the antibodies function as obstinance. And so what this means is that the antibodies will not be able to function as obstinance when pathogens have Fc receptors. And so pathogens with fc receptors are going to bind the antibodies and orient them in such a way where it's the F A. B region that is going to be pointing outwards instead of the fc region, like what normally happens and we'll be able to see this down below in our image. But since the F A B region is not an option in pathogens with Fc receptors will be able to avoid optimization and by avoiding optimization, they can also avoid fabulous itto sis. And so if we take a look at our image down below on the right hand side, notice that we're showing you a microbe with fc receptors, Fc antibody receptors so notice that the fc receptors are these little orange molecules that you see on the surface and notice that the fc receptors will bind to the fc region of the antibody and orient them in the opposite way that they're normally oriented. And so notice that the fC region is being bound to. So it's the F A B regions that are going to be pointing outwards And so the F A B region is not an obstinate. And so what that means is that this microbe here is going to be able to avoid optimization and fabio psychosis is going to fail. And so because fargo silicosis fails, the microbe has avoided to go silicosis by using these FC receptors. And so this year concludes our brief lesson on how some pathogens use FC receptors to prevent optimization and avoid fabio psychosis. And we'll be able to get some practice applying these concepts and learn more as we move forward, so I'll see you all in our next video.

Certain pathogens have Fc receptors on their surface to avoid which immune responses to infection?

• A. Opsonin proteins binding to the pathogen and triggering opsonization.
• B. C5a attracting phagocytic immune cells to the pathogen's location.
• C. Triggering the classical pathway of the compliment system.
• D. Release of histamines trigger an inflammatory response.

Why would some pathogens inhibit the functions of C3 convertase as a defense mechanism against the host's immune cells?

• A. To inhibit the formation of opsonin proteins that bind the pathogen.
• B. To inhibit the production of antibodies that recognize the pathogen.
• C. To inhibit the activation of T cells that trigger a larger immune response.
• D. To inhibit the differentiation of naive B cells into plasma cells.

Streptococcus pyogenes creates a C5a peptidase enzyme which breaks down the host's C5a proteins. Breaking down the C5a proteins has what result?

• A. Stopping the opsonization of Streptococcus pyogenes.
• B. Killing the phagocytic cells.
• C. Cell lysis of Streptococcus pyogenes.
• D. Inhibition of host's membrane attack complexes.
• E. Decreased accumulation of phagocytic immune cells.