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 26.7, Problem 1CR
Phagocytosis is the engulfing of infectious particles by phagocytes. Engulfed pathogens are bathed in toxic oxygen compounds inside the phagolysosome, killing and degrading them. However, some pathogens have developed various defense mechanisms to avoid or inhibit phagocytes, including secretion of leukocidins, the presence of a capsule, and biosynthesis of carotenoid pigments, which combat oxidative stress.
Explain how phagocytes kill microorganisms, with particular attention to oxygen-dependent mechanisms. Then identify at least three properties of pathogens that inhibit the effectiveness of phagocytes.
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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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Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- 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 themarrow_forwardTH2 cells coordinate type 2 responses to expel intestinal helminths and repair tissue injury. The immune response to helminthic worm infections in the gastrointestinal tract requires specialized mechanisms due to the fact that helminths are too large to be ingested and destroyed by phagocytes. For example, cytokines made by TH2 cells elicit responses from multiple non-hematopoietic cell types that aid in parasite expulsion. Name two of these cell types and for each of them, their response to TH2-produced cytokines.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_forward
- 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.arrow_forwardTrue/False: Neutrophils regulate the production of active cathelicidins (a class of antimicrobial peptides) by segregating the inactive propeptide from the processing enzyme that cleaves and activates it in two different types of cytoplasmic granules. These two types of granules are induced to fuse with phagosomes after ingestion of microbes, bringing the processing enzyme and the propeptide together.arrow_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
- Tumour associated macrophages (TAMS) represent up to 50% of cells in solid tumours. Explain how these cells contribute to immunosuppression in the tumour microenvironment and how they help tumour cells to evade anti-tumour immune responsesarrow_forwardDescribe how microfilaments and microtubules areinvolved in the phagocytosis and destruction of apathogen by a macrophage.arrow_forwardShigella, Mycobacterium, and numerous other pathogens have developed mechanisms that prevent them from being killed by phagocytes. Suggest 2 or 3 factors that help them avoid destruction by the powerful antiseptics in macrophages Suggest the potential implications that these infected macrophages can have on the development of diseasearrow_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_forwardA patient develops a blood infection with a capsule-producing strain of E. coli. Phagocytosis by macrophage will be essential to destroy the bacteria and resolve the infection. Which of the following will be dirertly required to allow ADCC-opsonization of the encapsulated E. coli: O Toll-like receptor (TLR)-induced secretion of tumor necrosis factor alpha O Release of C3a to the extracellular fluids O Presence of MHC II on the surface of the macrophage O Presence of IgG receptors (Fc-gamma-R) on the macrophage All of the answers applyarrow_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_forward
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