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 26.8, Problem 1CR
Fever and inflammation, characterized by pain, swelling (edema), redness (erythema), and heat, are normal and generally beneficial outcomes that result from activation of nonspecific immune response effectors. However, uncontrolled systemic inflammation, called septic shock, can lead to serious illness or death.
Identify the cells that initiate inflammation and the cells that are activated by inflammatory signals.
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During the chemotaxis phase of the inflammatory response,a. C-reactive protein is secreted by damaged parenchymal cells in the tissue, which attracts neutrophils, which secrete leukotrienes and prostaglandins to attract macrophages; a purulent exudate is formed.b. Band cells respond to hyperthermia by producing TNF-α and interleukins, which then cause a left shift that results in the accumulation of neutrophils within the tissue.c. Damaged parenchymal cells release prostaglandins and leukotrienes to attract macrophages, causing a left shift and the formation of a purulent exudate.d. Cytokines, such as TNF-α, are released by damaged parenchymal cells, while leukotrienes and prostaglandins produced by neutrophils cause smooth muscle constriction and the further accumulation of leukocytes.
In general, what are consequences of activation of the TH1 arm of the immune response? Activation of the TH2 arm?
Inflammation 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?
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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- True or False: The most abundant type of antibody, IgG, is the first to respond to an invading pathogen?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_forwardExplain why each choice (a-d) is correct or incorrect. All but one of the following occurs during the inflammatory response. Select the example below that does NOT describe the process of inflammation. a. Inflammation increases capillary permeability. b. Chemotaxis draws leucocytes to the site of injury. c. Vasoconstriction prevents excessive blood loss due to injury. d. Release of prostaglandins results in pain.arrow_forward
- Describe the cellular and vascular events of inflammation which lead to the four classic signs of inflammation. What role do cytokines play in acute inflammation? Please provide an example of a cytokine and its role in acute inflammationarrow_forwardList the types of exudate produced in inflammation.arrow_forwardMacrophages and neutrophils both contribute to extracellular pathogen protection. Describe their common characteristics, differences in structure and function, and if one were eliminated from the innate immune response, explain which one would be more detrimental to the body and why.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_forwardCompare and contrast innate and adaptive immunity. Include three similarities in terms of cell and/or cytokine actions and a discussion of the three hallmark differences (used to define each immune response).arrow_forwardDescribe an antibody-mediated response.arrow_forward
- Explain why each choice (a-d) is correct or incorrect. Which of the following examples below describes an autoimmune disease? a. Infection and death of T helper cells by a virus, resulting in a loss of adaptive immunity b. Release of bacterial endotoxins that block acetylcholine release result in muscle paralysis. c. Antibody binding to acetylcholine receptors of the motor end plate resulting in muscle weakness. d. Uncontrolled cell division resulting in cell surface abnormalities recognized by NK cells.arrow_forwardName two ways in which the presence of antibodies enhances phagocytosis.arrow_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
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