Brock Biology of Microorganisms, Books a la Carte Plus Mastering Microbiology with Pearson eText -- Access Card Package (15th Edition)
15th Edition
ISBN: 9780134603940
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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Students have asked these similar questions
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.
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.
In addition to phagocytosis, neutrophils use a process called NETs. Which one of the following describes this process?
Group of answer choices
A. NETs is a neutrophil process that activates the complement system of proteins, which destroys pathogens.
B. A net-like structure of DNA, histones, lactoferrins, gelatinase, cathepsin G, and myeloperoxidase is secreted at pathogens. Together these chemicals destroy pathogens.
C. NETs works when neutrophils secrete major basic proteins onto pathogens, destroying the pathogens' cell membranes.
D. NETs are chemicals secreted by neutrophils that trigger the rapid maturation of lymphoid stem cells into lymphocytes.
Chapter 26 Solutions
Brock Biology of Microorganisms, Books a la Carte Plus Mastering Microbiology with Pearson eText -- Access Card Package (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_forwardIt is often helpful to draw a complicated pathway in the form of a flow chart to visualize the multiple steps and the ways in which the steps are connected to each other. Draw the antibody-mediated immune response pathway that acts in response to an invading virus.arrow_forwardWhat is the difference between innate immunity and adaptive immunity?arrow_forward
- If 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_forwardIngestion 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 phagocytesarrow_forwardMultiple 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…arrow_forward
- Opsonization of pathogens by both antibodies and complement proteins (C3b) leads to uptake and destruction of the pathogen by phagocytic cells that express both Fc receptors and complement receptors. Which of the following in the figure below is the most efficient form of dual opsonization of the pathogen by antibody and C3b to maximize phagocytosis?arrow_forwardB cells express a complement receptor that binds to C3b cleavage products, such as iC3b and C3dg. When a B cell with an antigen receptor that specifically recognizes that pathogen also has its complement receptor stimulated because the pathogen is opsonized with these C3 fragments, B cell activation is greatly enhanced. Due to this mechanism, B cells can be activated by much lower concentrations of antigen (in this case, the pathogen) than if the antigen is devoid of complement components. This mechanism functions to: Ensure that pathogens are readily detected by the adaptive immune system before they replicate to high levels in the host Prevent B cells from being activated in response to antigens that are not pathogens Allow B cells to phagocytose the pathogen and help destroy it Induce increased rounds of B cell replication to make more pathogen-specific B cells Allow the B cell to block pathogen replication by interfering with multiple pathogen surface functionsarrow_forwardThe 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_forward
- Describe the roles that phagocytic and nonphagocytic cells and plasma proteins such as complement and interferon play in innate immunity?arrow_forwardInflammation is the hallmark of an activated immune response. Explain how inflammation is triggered by both innate and adaptive immune mechanisms. Are the inflammatory cells the same for both methods of activation? Why does inflammation subside as an infection is controlled?arrow_forwardWhich of the following is true about complement? Check all that apply. Three pathways of complement, where classical and alternative, are activated by antibodies and lectin by spontaneous hydrolysis of C3 Complement pathways are activated in response to infections and involved in opsonization, phagocytosis and lysis of microbes The"b" subunit of complement such as C3b or C5b is deposited on the microbes, whereas the "a" subunit, C3a or C5a recruits phagocytic cells to the site of infection and promotes inflammation Alternative pathway is activated immediately due to presence of C3b because of spontaneous hydrolysis of C3, whereas classical pathways in several days after secretion of pathogen-specific antibodies Seven complement(C) proteins are made by liver and C5 is found in abundancearrow_forward
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