Microbiology: An Evolving Science (Fourth Edition)
4th Edition
ISBN: 9780393615098
Author: John W. Foster, Joan L. Slonczewski
Publisher: W. W. Norton & Company
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Chapter 23.6, Problem 1TQ
Summary Introduction
To review:
The advantage of the H factor in bacteria.
Introduction:
The series of 20 proteins naturally found in serum form the complement. The complement pathway is the cascade process that attacks foreign invaders by enhancing the effect of antibodies. The complement system induces pores in the bacterial membrane leading to cytoplasmic leakage. Sometimes the pathogen can take advantage of these controls to avoid being destroyed by the immune system of the human body.
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4) A patient has their spleen removed due to an accident. How will this affect the immune response?
5) You come in contact with staphylococci through a cut. What cellular features will the immune cells recognize?
6) Name two opsonins and how do these molecules help the immune response?
7) Fever is part of the inflammatory process. What is the role of fever during an immune response?
8) This chemical is used to induce anti-viral responses in cells to protect the cells from viral infections.
9) This complement activation pathway is activated when complement binds to an antibody bound to antigens.
Mannose binding lectins (MBL) and ficolins are the two classes of proteins that can initiate the lectin pathway of complement activation. These proteins are selective for activating complement on the surfaces of microbial pathogens rather than host cells because:
Their higher-order oligomeric structure can be assembled only after the monomers first bind to pathogen membranes.
They only recruit MASP (MBL-associated serine proteases) proteins when bound to pathogen surfaces and not when bound to host cells.
They only undergo the conformational change needed to activate MASP proteins when bound to a pathogen and not when bound to a host cell.
They only bind to carbohydrate side chains and oligosaccharide modifications found on pathogen surfaces but not on host cell membranes.
The activated MASP proteins are rapidly inactivated by hydrolysis when present on the surface of a host cell.
Mycobacteria are intracellular pathogens that have adapted to life inside phagocytic cells, such as macrophages. These intracellular bacteria are taken up by phagocytosis, similar to other pathogens, but the bacteria are not killed. One possible mechanism that could account for this immune evasion by mycobacteria is their ability to:
Prevent induction of nitric oxide production in the phagosome
Prevent the acidification of phagosomes
Prevent the expression of antimicrobial peptides in the phagosome
Prevent fusion of phagosomes with lysosomes
Kill the macrophage before it kills them
Chapter 23 Solutions
Microbiology: An Evolving Science (Fourth Edition)
Ch. 23.1 - Prob. 1TQCh. 23.1 - Prob. 2TQCh. 23.1 - Prob. 3TQCh. 23.3 - Prob. 1TQCh. 23.4 - Prob. 1TQCh. 23.5 - Prob. 1TQCh. 23.5 - Prob. 2TQCh. 23.5 - Prob. 3TQCh. 23.6 - Prob. 1TQCh. 23.6 - Prob. 2TQ
Ch. 23 - Prob. 1RQCh. 23 - Prob. 2RQCh. 23 - Prob. 3RQCh. 23 - Prob. 4RQCh. 23 - Prob. 5RQCh. 23 - Prob. 6RQCh. 23 - Prob. 7RQCh. 23 - Prob. 8RQCh. 23 - Prob. 9RQCh. 23 - Prob. 10RQCh. 23 - Prob. 11RQCh. 23 - Prob. 12RQCh. 23 - Prob. 13RQCh. 23 - Prob. 14RQCh. 23 - Prob. 15RQCh. 23 - Prob. 16RQCh. 23 - Prob. 17RQCh. 23 - Prob. 18RQCh. 23 - Prob. 1TQCh. 23 - Prob. 2TQCh. 23 - Prob. 3TQ
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- The formation of the C3 convertase is a key step in complement activation that occurs in all three complement pathways. This enzyme cleaves C3 in blood plasma, leading to a conformational change in the C3b fragment that exposes its reactive thioester group. The activated C3b is potentially harmful to the host, if it becomes covalently attached to a host cell, rather than to the surface of a pathogen. This deleterious outcome is largely avoided by: The inability of active C3b to diffuse away in the blood plasma. The inability of active C3b to covalently attach to the membranes of eukaryotic cells. The rapid hydrolysis of active C3b in solution, rendering it inactive. The tight binding of active C3b to the C3 convertase. The ability of active C3b to recruit phagocytic cells.arrow_forwardSome bacterial cells avoid the killing effects of activated complement proteins. How might they do this?arrow_forwardAlthough the complement cascade can be initiated by antibodies bound to the surface of a pathogen, complement activation is generally considered to be an innate immune response. This is because: Two of the three pathways for complement activation are initiated by constitutively produced recognition molecules that directly interact with microbial surfaces. When the complement cascade leads to the formation of a membrane-attack complex, the pathogen is killed. Several of the soluble products generated by complement activation lead promote the inflammatory response. Complement proteins bound to the pathogen promote uptake and destruction by phagocytic cells. The C3 convertase is only produced when complement activation is initiated by antibody binding to a pathogen.arrow_forward
- Which of these does NOT describe complement? It is a type of antibody. It is an innate (non-specific) immune response. It can be activated by contact with the microbe’s cell surface. It destroys bacterial cells by lysis and by enhancing phagocytosis. It is a group of proteins found in the blood.arrow_forwardMACS are donut-shaped protein complexes of the complement system that create holes in bacterial cells to cause apoptosis. O 1) True O 2) Falsearrow_forwardIn HIV, helper T cells are affected. Describe how this impacts both the humoral and cell- mediated immune system. Why would an ordinary cold virus be dangerous to an AIDS patient?arrow_forward
- The classical complement pathway is initiated by C1q binding to the surface of a pathogen. In some cases, C1q can directly bind the pathogen, for instance by recognizing proteins of bacterial cell walls, but in most cases C1q binds to IgM antibodies that are bound to the pathogen surface. How does this IgM-binding feature of C1q contribute to rapid, innate immune responses rather than to slow, adaptive responses? C1q induces B lymphocytes to begin secreting antibody within hours of pathogen exposure. Natural antibody that binds to many microbial pathogens is produced prior to pathogen exposure. C1q binds to C-reactive protein which then binds to IgM on the pathogen surface. C1q directly induces inflammation, recruiting phagocytes and antibodies from the blood into the infected tissue. C1q binds to dendritic cells in the infected tissue, inducing them to secrete inflammatory cytokines.arrow_forwardWhich of the following complement components are generated during the classical pathway and bind independently to the membrane surface promoting immune adherence and opsonizing effects? C3b O C3d O C1q O C2arrow_forwardNeutralizing antibodies are effective at preventing infection or toxicity mediated by pathogens or their toxic products. In fact, nearly all vaccines currently in use function by eliciting neutralizing antibodies. One example is the tetanus vaccine, in which neutralizing antibodies are generated against an inactivated form of the tetanus toxin (the tetanus toxoid). The most important feature of a neutralizing antibody is having high affinity for the antigen. being efficient at activating the complement cascade. having a high degree of multivalency, such as being a pentamer or hexamer of immunoglobulin monomers. being present at a high concentration in the circulation. 0 0 0 0arrow_forward
- What does innate mean? How is the innate immune system different from the adaptive immune system? Compare the strategies of innate immunity with strategies of adaptive immunity. Give specific examples. How do vaccines protect us from diseases? Which cells in the immune system become activated after the injection? Your answer should be written as 2 or more paragraphs with a total word count of 400 or more.arrow_forwardComplement could be one example of a ?????, one of the three types of defenses employed by the innate immune system.arrow_forwardInhibitory receptors on lymphocytes down-regulate immune responses by recruiting protein or lipid phosphatases.BCR signaling on B cells is initiated by antigen binding, leading to mTOR activation. This occurs, for instance, when the antigen is a live microbe that binds to the BCR on the B cells. Which one of the forms of antigen shown below the graph would correctly account for the data shown in the figure?arrow_forward
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