Pathology and Pathogenesis of Bacterial Infections

Steffen Stenger; Robert Modlin

doi:10.1128/9781555817978.ch20

Chapter 20 : Pathology and Pathogenesis of Bacterial Infections

Authors: Steffen Stenger¹, Robert Modlin²

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Affiliations: 1: Institut für Klinische Mikrobiologie, Immunologie und Hygiene, Friedrich-Alexander Universität Erlangen-Nürnberg, D-91054 Erlangen, Germany; 2: Division of Dermatology and Department of Microbiology and Immunology, UCLA School of Medicine, Los Angeles, CA 90095

Content Type: Monograph

Publication Year: 2002

Category: Immunology

Book DOI: 10.1128/9781555817978

Chapter DOI: 10.1128/9781555817978.ch20

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Abstract:

This chapter provides a classification of relevant immunopathological reactions depending on the underlying mechanisms leading to tissue damage. The release of mediators such as histamine, leukotrienes, and heparin from mast cells accounts for the anaphylactic reactions to horse serum or to penicillin but is usually not important in the immunopathology of bacterial infections. CD8+ T cells may contribute to host resistance by at least four mechanisms: (i) release of IFN-γ, (ii) lysis of the target cell, (iii) induction of apoptosis of the target cells, and (iv) mediation of direct antimicrobial activity. This chapter provides a brief outline of the immunoprotective and immunopathological features of these mechanisms, using tuberculosis as an example. Cytokines therefore play an important role in immune defense but also contribute to immunopathology and disease. Although tumor necrosis factor (TNF) is crucial to the protective immune response, it also plays a part in the immunopathology of tuberculosis. The typical clinical syndrome, in conjunction with knowledge about the pathophysiology of septic shock, has supported the hypothesis that TNF is released at the onset of antimycobacterial therapy and mediates immunopathology. Mechanistically, one could argue that harmful effects may be ascribed to the biological activity of TNF in affecting vascular endothelium by inducing procoagulant activity, formation of thrombi, and production of nitric oxide synthase, thus causing endarteritis. Rheumatic fever is the most commonly cited example of molecular mimicry in humans.

Citation: Stenger S, Modlin R. 2002. Pathology and Pathogenesis of Bacterial Infections, p 281-292. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch20

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