Brock Biology of Microorganisms (15th Edition)
15th Edition
ISBN: 9780134261928
Author: Michael T. Madigan, Kelly S. Bender, Daniel H. Buckley, W. Matthew Sattley, David A. Stahl
Publisher: PEARSON
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Chapter 26.9, Problem 1CR
The complement system is composed of soluble proteins that catalyze bacterial opsonization and cell lysis. Complement is triggered by antibody interactions or by interactions with nonspecific activators, such as mannose-binding lectin. Complement activation may be a product of either innate or adaptive immunity. Complement may enhance phagocytosis, cause target cell lysis, or induce an inflammatory response.
Describe the complement system. Is the order of protein interactions important? Why or why not? Identify the components of the mannose-binding lectin pathway for complement activation. Identify the components of the alternative pathway for complement activation. How do these complement activation pathways differ from the classical pathway?
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Although 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.
Ingestion of complement-tagged pathogens by phagocytes is mediated by receptors for the bound complement proteins. Even when the complement cascade fails to proceed beyond generating the C3 convertase, complement activation is effective at inducing pathogen uptake and destruction. This process of immune protection is mediated by:
Activation of complement inhibitory receptors on phagocytes that promote pathogen uptake
Activation of soluble proteases in the serum that disrupt pathogen membranes
Engagement of complement receptors on phagocytes by C3b and its cleavage products which promotes phagocytosis
Engagement of complement receptors on B cells that promotes antibody production
Stimulation of antimicrobial peptide secretion by phagocytes
Multiple pathways for regulating complement activation limit the potential damage caused by complement deposition on host cells or caused by the spontaneous activation of complement proteins in the plasma. Genetic deficiencies in these mechanisms often lead to chronic inflammatory diseases, but in some cases can paradoxically lead to increased susceptibility to bacterial infections. This latter outcome may occur because:
Complement regulatory proteins have dual functions in inhibiting and promoting complement activation.
Uncontrolled complement activation leads to the depletion of serum complement proteins.
The inhibition of the membrane attack complex by complement regulatory proteins normally leads to enhanced activation of the early steps of the complement pathway.
Complement regulatory proteins normally cause the rapid depletion of plasma complement factors.
Uncontrolled complement activation recruits the majority of phagocytic cells, leaving few remaining to fight infections in…
Chapter 26 Solutions
Brock Biology of Microorganisms (15th Edition)
Ch. 26.1 - What major class of immune cells mediates an...Ch. 26.1 - Prob. 2MQCh. 26.1 - Compare and contrast the major features of innate...Ch. 26.2 - Describe host tissue specificity for pathogens.Ch. 26.2 - Identify physical and chemical barriers to...Ch. 26.2 - What other factors may control the outcome of an...Ch. 26.2 - Identify at least four mechanisms by which a...Ch. 26.3 - Describe the circulation of a leukocyte from the...Ch. 26.3 - What soluble molecules determine whether a...Ch. 26.3 - Cells involved in innate and adaptive immunity...
Ch. 26.4 - How does the development of B, T, and NK cells...Ch. 26.4 - Distinguish between the primary lymphoid organs...Ch. 26.4 - Leukocytes are differentiated white blood cells...Ch. 26.5 - Although technically not part of the immune...Ch. 26.5 - Describe the mechanisms by which circulating...Ch. 26.5 - Pathogens may colonize host tissues when...Ch. 26.6 - Identify a PAMP shared by a group of...Ch. 26.6 - Outline the general features of a signal...Ch. 26.6 - Innate recognition of common pathogens occurs...Ch. 26.7 - Identify the mechanism used by phagocytes to...Ch. 26.7 - Describe several reasons why phagocytes are not...Ch. 26.7 - Phagocytosis is the engulfing of infectious...Ch. 26.8 - Prob. 1MQCh. 26.8 - Identify the major symptoms of localized...Ch. 26.8 - Fever and inflammation, characterized by pain,...Ch. 26.9 - In what ways does the classical pathway of...Ch. 26.9 - What is opsonization, and how does opsonization...Ch. 26.9 - Why are the mannose-binding lectin and alternative...Ch. 26.9 - The complement system is composed of soluble...Ch. 26.10 - Prob. 1MQCh. 26.10 - Prob. 2MQCh. 26.10 - Prob. 1CRCh. 26 - Prob. 1AQCh. 26 - Describe the potential problems that would arise...Ch. 26 - Prob. 3AQCh. 26 - Prob. 4AQ
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- Complement proteins function in defense by _______. a. neutralizing toxins b. enhancing resident bacteria c. promoting inflammation d. forming pores that cause pathogens to disintegrate e. both a and b f. both c and darrow_forwardWhat is the difference between innate immunity and adaptive immunity?arrow_forwardIf a series of genetic mutations prevented some, but not all, of the complement proteins from binding antibodies or pathogens, would the entire complement system be compromised?arrow_forward
- Neutralizing 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_forwardMannose 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.arrow_forwardIgM antibodies are much more efficient than IgG at activating the complement cascade. However, under certain circumstances, IgG antibodies will activate the complement pathway. One example of a situation in which IgG binding to its antigen will not trigger the complement cascade is when the IgG antibodies are neutralizing a bacterial toxin protein by blocking the receptor-attachment site on the toxin. the IgG antibodies are binding self-antigens, such as chromatin released from dead cells. the IgG antibodies bind to a bacterial surface by recognizing a repetitive polysaccharide component of the bacterial capsule. the IgG antibodies bind to a viral capsid protein that is present in more than 100 copies on the viral particle surface.arrow_forward
- Individuals infected with herpes simplex virus (HSV) mount protective antibody responses directed against surface glycoproteins of the virus. These antibodies are critical to viral clearance. The act to neutralise any virus trying to infect a person’s cells as well as activating the classical pathway of complement and cytotoxic cell-mediated killing of infected target cells. Having a deficiency in the complement component C3 greatly impairs a person’s ability to control HSV infections. To understand this further, you will investigate this in the lab. Using C3-deficient mice, you infect them with HSV at day 0 and then a second time 4 weeks later. A hypothesis is a tentative answer to a scientific question and is an important part of practical experiments. A testable hypothesis is statement that can be proved or disproved as a result of experimentation. Q1. State the problem that you are trying to solve. And then formulate a robust testable hypothesis for your…arrow_forwardIndividuals infected with herpes simplex virus (HSV) mount protective antibody responses directed against surface glycoproteins of the virus. These antibodies are critical to viral clearance. The act to neutralise any virus trying to infect a person’s cells as well as activating the classical pathway of complement and cytotoxic cell-mediated killing of infected target cells. Having a deficiency in the complement component C3 greatly impairs a person’s ability to control HSV infections. To understand this further, you will investigate this in the lab. Using C3-deficient mice, you infect them with HSV at day 0 and then a second time 4 weeks later. A hypothesis is a tentative answer to a scientific question and is an important part of practical experiments. A testable hypothesis is statement that can be proved or disproved as a result of experimentation. You perform an ELISA to measure the antibody response of the C3-deficient and normal mice (referred to as wild-type – WT)…arrow_forwardThe 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_forward
- The terminal complement proteins polymerize to form pores in membranes that can kill certain pathogens. The terminal components of the complement pathway assemble to form a membrane attack complex that can induce pathogen lysis and death. Yet, evidence indicates that this feature of complement is less important than the earlier steps that promote pathogen opsonization and induce inflammation. This conclusion is based on: In vitro experiments showing that very few species of bacteria are susceptible to lysis by the membrane attack complex Experiments indicating that only bacteria, but not viruses or fungi, are susceptible to lysis by the membrane attack complex The very low levels of terminal complement components in the serum The fact that other mammalian species lack the terminal components of the complement pathway needed to form the membrane attack complex The limited susceptibility to infections of patients with deficiencies in terminal complement componentsarrow_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_forwardPathogens produce several types of proteins that can inhibit complement activation. The importance of complement activation as an innate immune defense against infections is illustrated by: The evolution of complement avoidance strategies by many pathogens The large number of proteins involved in the complement pathway The large number of complement regulatory pathways expressed by the host The existence of three different mechanisms for initiating complement activation The ability of the membrane attack complex to lyse some pathogensarrow_forward
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