4) Avoiding Complement System - Online Tutor, Practice Problems & Exam Prep

Some pathogens, known as serum resistant bacteria, have evolved mechanisms to evade the complement system of innate immunity. They achieve this by binding to and inhibiting the complement protein C3b, preventing the formation of C3 convertase, which is crucial for activating the complement system. Without this activation, processes like inflammation, opsonization, and membrane attack complexes are inhibited, allowing these bacteria to resist destruction. Understanding these mechanisms is vital for developing effective treatments against such resistant pathogens.

Avoiding Complement System

In this video, we're going to talk about how some pathogens have evolved mechanisms for avoiding the complement system of innate immunity. Recall from some of our previous lesson videos that the complement system activation can result in inflammation, opsonization, or membrane attack complexes, also known as MACs. Activation of the complement system leads to the destruction and elimination of the pathogen. Some bacteria are resistant to the complement system because they can prevent activation of the complement system. These bacteria that are resistant are specifically called serum resistant bacteria. The term serum refers to the specific component of the blood where the complement proteins reside. Serum-resistant bacteria can prevent complement system activation and therefore they're able to prevent their own destruction and elimination by binding and inhibiting the complement system protein C3b. Recall that C3b is a complement system protein important for activating the rest of the complement system. The regulatory proteins on serum-resistant bacteria are the ones that bind and inhibit C3b, preventing C3 convertase formation, which ultimately prevents activation of the complement system.

If we take a look at our image, we can get a better understanding of the complement system and serum-resistant bacteria. Notice that our image is broken up into two regions. The top region with the greenish background and the bottom region with a reddish background. In the top region, where there is no regulatory protein, this represents a cell without the regulatory protein. This would just be a normal bacterial cell, not a serum-resistant bacterial cell. Without this regulatory protein, C3b is able to bind to the bacterial cell surface and will associate with other complement system proteins. When C3b binds with other complement system proteins forming C3 convertase, it leads to the activation of the complement system. Activation of the complement system leads to inflammation, opsonization, or membrane attack complexes, and this bacterial cell would be eliminated. However, in the bottom region with the reddish background, we are looking at the serum-resistant bacteria, which most of this text focuses on. These serum-resistant bacteria have a regulatory protein. The serum-resistant regulatory protein binds to C3b and blocks and inhibits it, preventing C3b from interacting with other complement proteins. When C3b is bound by the regulatory protein, other complement system proteins are unable to interact with it. C3b is blocked, and it will not be able to form C3 convertase. If C3 convertase is not formed, there will be no activation of the complement system. This means that inflammation, opsonization, and membrane attack complexes will not occur. The serum-resistant bacteria are able to resist the complement system and prevent its activation as discussed. This concludes our lesson on how some pathogens avoid the complement system, specifically serum-resistant bacteria, and we will practice applying these concepts as we move forward. I'll see you all in our next video.

Which types of pathogenic bacteria are susceptible to MACs and why?

• A. Gram-positive bacteria because MACs easily pass through the thick cell wall to reach the plasma membrane.
• B. Gram-negative bacteria because the MACs attack their outer membrane which is not protected by the cell wall.
• C. Both gram-negative and gram-positive bacteria are susceptible to MACs.

All of these survival mechanisms are unique to serum resistant bacterial pathogens except which of the following?

• A. Producing membrane damaging toxins.
• B. Bacterial proteins binding to C3b.
• C. Thick peptidoglycan cells walls.
• D. Inhibition of C3 convertase.

Here’s what students ask on this topic:

What are serum resistant bacteria and how do they avoid the complement system?

Serum resistant bacteria are pathogens that have evolved mechanisms to evade the complement system of innate immunity. They achieve this by binding to and inhibiting the complement protein C3b. This inhibition prevents the formation of C3 convertase, which is crucial for activating the complement system. Without C3 convertase, the processes of inflammation, opsonization, and membrane attack complexes (MACs) are not initiated. Consequently, these bacteria can resist destruction and elimination by the immune system. Understanding these mechanisms is essential for developing effective treatments against such resistant pathogens.

How does the complement protein C3b contribute to the activation of the complement system?

The complement protein C3b plays a pivotal role in the activation of the complement system. When C3b binds to the surface of a pathogen, it associates with other complement proteins to form C3 convertase. C3 convertase is an enzyme complex that catalyzes the cleavage of more C3 molecules, amplifying the response. This activation leads to processes such as inflammation, opsonization (marking pathogens for phagocytosis), and the formation of membrane attack complexes (MACs) that can lyse and destroy pathogens. Therefore, C3b is essential for the proper functioning of the complement system.

What role do regulatory proteins play in serum resistant bacteria?

Regulatory proteins on the surface of serum resistant bacteria play a crucial role in evading the complement system. These proteins bind to the complement protein C3b, inhibiting its interaction with other complement proteins. This inhibition prevents the formation of C3 convertase, which is necessary for the activation of the complement system. By blocking C3b, these regulatory proteins ensure that processes like inflammation, opsonization, and membrane attack complexes (MACs) are not initiated, allowing the bacteria to avoid destruction by the immune system.

Why is the formation of C3 convertase important in the complement system?

The formation of C3 convertase is a critical step in the activation of the complement system. C3 convertase is an enzyme complex that cleaves the complement protein C3 into C3a and C3b. This cleavage amplifies the complement response, leading to the recruitment of immune cells (inflammation), marking pathogens for phagocytosis (opsonization), and the formation of membrane attack complexes (MACs) that can lyse and destroy pathogens. Without C3 convertase, these essential immune responses cannot occur, making it a key target for serum resistant bacteria to evade the immune system.

How do serum resistant bacteria impact the effectiveness of the immune system?

Serum resistant bacteria impact the effectiveness of the immune system by evading the complement system, a crucial component of innate immunity. By binding to and inhibiting the complement protein C3b, these bacteria prevent the formation of C3 convertase, which is essential for activating the complement system. Without this activation, processes like inflammation, opsonization, and membrane attack complexes (MACs) are inhibited. This allows serum resistant bacteria to avoid destruction and elimination, making it challenging for the immune system to effectively combat these pathogens. Understanding these mechanisms is vital for developing treatments against such resistant bacteria.