2) Avoiding Phagocytosis - Online Tutor, Practice Problems & Exam Prep

Pathogens have evolved various strategies to evade phagocytosis, including the production of C5a peptidase, which degrades the complement protein C5a, preventing phagocyte recruitment. Additionally, some pathogens utilize membrane-damaging toxins to lyse phagocytic cells. Others avoid opsonization through capsules that block opsonins like C3b, or by producing M proteins that inhibit C3 convertase, thus preventing opsonin production. Furthermore, pathogens with Fc receptors can reorient antibodies, hindering their opsonizing function, ultimately allowing these pathogens to escape immune detection and destruction.

Pathogens Avoid Encounter with Phagocytes

In this video, we're going to talk about how some pathogens have evolved mechanisms of avoiding phagocytosis in order to avoid the immune system. First, we need to recall from some of our previous lesson videos that we discussed the process of phagocytosis in detail. Recall from those older videos that phagocytic cells are able to destroy microbes in a series of steps that involves chemotaxis, recognition, attachment, engulfment, and fusion. If you don't remember these steps of phagocytosis, be sure to check out those videos before you continue here. Now that being said, some pathogens once again have evolved mechanisms of avoiding an encounter with phagocytes. Certain pathogens can avoid encountering phagocytic cells by using one of two mechanisms that we have numbered below, 1 and 2.

The first mechanism of avoiding an encounter with phagocytes is through the production of the enzyme called C5a peptidase. Peptidases are enzymes because they end in "ase" that are going to break peptide bonds or break down proteins. C5a peptidase is an enzyme that breaks down the protein C5a. So it degrades the complement system protein C5a. You might recall from some of our previous lesson videos when we discussed the complement system, that C5a is a complement system protein that serves as a chemoattractant in order to recruit phagocytic cells to the site of infection. By breaking down the protein C5a, phagocytic cells will not be recruited to the site of infection, and that can allow a pathogen to avoid an encounter with the phagocyte. Notice that this blue microbe on the left-hand side is producing an enzyme called C5a peptidase, and C5a peptidase, which is produced by this pathogen, can degrade the protein C5a. By degrading C5a, there will be no C5a to serve as a chemoattractant to recruit the phagocytic cell. Because there's no recruitment of the phagocytic cell, the pathogen can avoid an encounter with the phagocytic cell. Notice that this macrophage is saying, "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 a phagocyte.

The second way is through the production of membrane-damaging toxins. Membrane toxins, as their name implies, are going to be toxins that cause damage to the membrane. They can kill phagocytes and other cells as well. They can actually form pores or holes in the membranes of phagocytic cells and cause those phagocytic cells to lyse or rupture. Notice that in our image on the right-hand side, we're showing you how some pathogens can produce membrane-damaging toxins to avoid an encounter with a phagocyte. Here we have a microbe, a pathogen, and this pathogen is producing and releasing these little pink molecules that are membrane-damaging toxins. The membrane-damaging toxins can again cause damage to the membrane of the phagocytic cell, create pores or holes in the membrane of the phagocytic cell, and that can also ultimately lead to the lysis or lysed phagocytic cell, a lysed macrophage for example. This is going to allow the pathogen to avoid an encounter with the macrophage.

It is also important to note that some pathogens have evolved the ability to survive phagocytosis by phagocytic cells and induce apoptosis once they're inside the cell. It could be a process similar to this except the pathogen would actually be engulfed. Once the pathogen is engulfed, it would then cause the phagocytic cell to undergo apoptosis. This concludes our brief lesson on how some pathogens have the ability to avoid an encounter with phagocytes. As we move forward, we'll talk about other methods of avoiding phagocytosis. We'll get to talk about those other methods as we move forward. 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.

Pathogen Use Capsules & M Proteins to Avoid Opsonization

In this video, we're going to continue to talk about how some pathogens can avoid phagocytosis by talking specifically about how some pathogens can use capsules and M proteins to avoid opsonization. And so first we need to recall from some of our previous lesson videos what the term Opsonization means. And so recall that Opsonization refers to the process that makes microbes easier to bind or engulf during phagocytosis. And so once again, some pathogens can prevent opsonization. By preventing opsonization, they make phagocytosis more difficult and therefore they can avoid phagocytosis. Some pathogens are able to prevent opsonization by the production of a capsule. 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. These capsules can prevent immune cells and opsinins like the complement protein C3b from adhering to the pathogen. By preventing immune cells and opsinins from adhering to the pathogen, that will avoid opsonization and again avoid phagocytosis.

Now, very similar to capsules, the production of the cell wall protein called the M protein can also allow a pathogen to avoid opsonization. What happens is the M protein will bind to another regulatory protein or inhibitory protein that is going to be degrading the enzyme C3 Convertase which is important for complement system activation. By degrading C3 Convertase, that is going to inhibit or block the production of C3b, the complement protein C3b, which again we know acts like an opsinin. If we take a look at our image down below, we'll be able to get a better understanding of this idea. Notice on the left hand side, we're showing you how capsules can block C3b binding. Notice that we have two microbes. We have this microbe on the left that is in blue, and then we have the microbe that's on the right. Notice that the microbe that is on the left does not have a capsule. Because it does not have a capsule, the opsonin protein C3b is capable of binding to the surface of that microbe, and therefore opsonization will take place and that means that this microbe is likely to be engulfed through the process of phagocytosis. 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. This outer capsule can block the binding of C3b. So C3b cannot bind. If C3b cannot bind, what that means is that there is no opsonization. By preventing opsonization with the capsule, that is going to allow it to avoid phagocytosis.

Now, on the right hand side, we're showing you how the M protein can block C3 convertase. What you'll notice is that the cell over here on the left is producing this M protein on its cell wall. This M protein will associate with an inhibitory protein, this little purple structure or a regulatory protein, and the inhibitory protein will basically degrade C3 convertase. You might recall when we covered the complement system in some of our previous lesson videos that C3 convertase is an enzyme that is important for complement system activation. By degrading C3 Convertase, C3 Convertase is going to be blocked, and it will be blocked from making the opsinin C3b, from C3. Usually what happens is C3 convertase will be involved with converting C3 into C3a and C3b and then C3b would serve as an opsinin. However, if there is M protein, that means it will associate with the inhibitory protein. The inhibitory protein blocks C3 convertase, and then what that means is C3 will not be converted into C3b. By blocking C3 convertase, it is blocking the production of an opsinin, and that is going to avoid opsonization, and that will avoid phagocytosis.

This here concludes our brief lesson on how pathogens can use capsules and M proteins to avoid opsonization and therefore avoid phagocytosis. 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.

Pathogens Use Fc Receptors to Prevent Opsonization

In this video, we're going to talk about how some pathogens can use the Fc antibody receptors to prevent opsonization and therefore avoid phagocytosis. So first, we need to recall from some of our previous lesson videos the typical structure of an antibody is a Y shape just like what you see down below. And within this typical structure of the antibody, we have the FAB 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 opsonin for phagocytes. And the FAB 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 antigen-binding regions binding to the pathogen and their Fc regions pointing outwards away from the pathogen. That will allow for phagocytosis 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 opsonins. And so what this means is that the antibodies will not be able to function as opsonins 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 FAB 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 FAB region is not an opsonin, pathogens with Fc receptors will be able to avoid opsonization, and by avoiding opsonization, they can also avoid phagocytosis.

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 FAB regions that are going to be pointing outwards. And so the FAB region is not an opsonin. And so what that means is that this microbe here is going to be able to avoid opsonization, and phagocytosis is going to fail. And so because phagocytosis fails, the microbe has avoided phagocytosis by using these Fc receptors. And so this here concludes our brief lesson on how some pathogens use Fc receptors to prevent opsonization and avoid phagocytosis, 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.

Here’s what students ask on this topic:

What are the mechanisms pathogens use to avoid phagocytosis?

Pathogens have evolved several mechanisms to avoid phagocytosis. One method is the production of C5a peptidase, which degrades the complement protein C5a, preventing the recruitment of phagocytes. Another strategy involves the production of membrane-damaging toxins that lyse phagocytic cells. Additionally, some pathogens use capsules to block opsonins like C3b, preventing opsonization. M proteins can also inhibit C3 convertase, reducing opsonin production. Lastly, pathogens with Fc receptors can reorient antibodies, hindering their opsonizing function and allowing the pathogen to evade immune detection.

How do capsules help pathogens avoid phagocytosis?

Capsules help pathogens avoid phagocytosis by preventing opsonization. Capsules are outer layers composed of carbohydrates and proteins that surround the bacterial cell. They block opsonins like the complement protein C3b from binding to the pathogen's surface. Without opsonins, phagocytic cells find it more difficult to recognize and engulf the pathogen, allowing it to evade the immune response. This mechanism is crucial for pathogens to survive and proliferate within the host.

What role do Fc receptors play in avoiding phagocytosis?

Fc receptors on pathogens play a significant role in avoiding phagocytosis by binding to the Fc region of antibodies. Normally, the Fc region points outward and serves as an opsonin, facilitating phagocytosis. However, when pathogens have Fc receptors, they bind to the Fc region, reorienting the antibody so that the Fab region points outward. Since the Fab region is not an opsonin, this reorientation prevents the antibody from aiding in phagocytosis, allowing the pathogen to evade immune detection and destruction.

How do membrane-damaging toxins help pathogens evade phagocytosis?

Membrane-damaging toxins help pathogens evade phagocytosis by lysing phagocytic cells. These toxins create pores or holes in the membranes of phagocytes, leading to cell lysis or rupture. By killing the phagocytic cells, the pathogens prevent their own engulfment and destruction. This mechanism allows the pathogens to survive and proliferate within the host, evading the immune response effectively.

What is the function of C5a peptidase in avoiding phagocytosis?

C5a peptidase is an enzyme produced by some pathogens to avoid phagocytosis. It degrades the complement protein C5a, which is crucial for recruiting phagocytic cells to the site of infection. By breaking down C5a, the enzyme prevents the chemoattractant signal that would normally draw phagocytes to the pathogen. This allows the pathogen to evade an encounter with phagocytic cells, thereby avoiding phagocytosis and subsequent destruction by the immune system.