Brock Biology of Microorganisms (15th Edition)
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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Therapeutic agents are currently being investigated that block the action of selectins in order to prevent the pathological effects resulting from leukocyte entry into sites of inflammation. These agents are molecules that inhibit selectin. Describe molecules that might be effective. (Information: Glycoproteins are an important class of proteins. There are many families of glycoproteins: lectins and selectins are examples.)
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.
IgM 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.

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Brock Biology of Microorganisms (15th Edition)

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