Ch. 16 - Innate Immunity: Nonspecific Defenses of the Host

Tortora - Microbiology: An Introduction 14th Edition

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Tortora 14th Edition

Ch. 16 - Innate Immunity: Nonspecific Defenses of the Host

Problema 4

Capitolo 12, Problema 4

How can the complement system cause endotoxic shock?

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Understand that the complement system is a part of the innate immune response, consisting of proteins that, when activated, enhance inflammation, opsonization, and cell lysis.

Recognize that endotoxic shock is caused by the presence of endotoxins, such as lipopolysaccharides (LPS) from the outer membrane of Gram-negative bacteria, in the bloodstream.

Explain that endotoxins can activate the complement system, particularly through the alternative pathway, leading to the generation of potent inflammatory mediators like C3a and C5a, known as anaphylatoxins.

Describe how these anaphylatoxins increase vascular permeability, cause vasodilation, and recruit immune cells, which can lead to widespread inflammation and a drop in blood pressure characteristic of shock.

Summarize that excessive or uncontrolled activation of the complement system by endotoxins results in systemic inflammation, contributing to the pathophysiology of endotoxic shock.

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Complement System Activation

The complement system is a group of proteins in the blood that, when activated, enhance immune responses by promoting inflammation, opsonization, and cell lysis. It can be triggered by pathogens or their components, such as endotoxins, leading to a cascade that amplifies immune defense.

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05:15

Review of the Complement System

Endotoxins and Their Role

Endotoxins are lipopolysaccharides (LPS) found in the outer membrane of Gram-negative bacteria. When released into the bloodstream, they trigger strong immune responses, including activation of the complement system, which can lead to widespread inflammation and tissue damage.

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02:46

Endotoxin

Mechanism of Endotoxic Shock

Endotoxic shock occurs when excessive complement activation by endotoxins causes massive release of inflammatory mediators like cytokines and anaphylatoxins. This results in systemic vasodilation, increased vascular permeability, and hypotension, potentially leading to multi-organ failure and death.

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01:59

Introduction to Avoiding Host Defense Mechanisms

Pratica correlata

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A human host can prevent a pathogen from getting enough iron by all of the following except

a. reducing dietary intake of iron.

b. binding iron with transferrin.

c. binding iron with hemoglobin.

d. binding iron with ferritin.

e. binding iron with siderophores.

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If the following are placed in the order of occurrence, which would be the third step?

a. Activation of C5 through C9

b. Cell lysis

c. Antigen–antibody reaction

d. Activation of C3

e. Activation of C2 through C4

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Patients with X-linked chronic granulomatous disease are susceptible to infections because their neutrophils don’t generate an oxidative burst. What is the relation of the oxidative burst to infection?

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Define inflammation, and list its characteristics.

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If the following are placed in the order of occurrence, which would be the third step?

a. Diapedesis

b. Digestion

c. Formation of a phagosome

d. Formation of a phagolysosome