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7 - Bacterial toxins that modify the epithelial cell barrier

from Part II - Bacterial cell biology and pathogenesis

Published online by Cambridge University Press:  12 August 2009

Joseph T. Barbieri
Affiliation:
Medical College of Wisconsin, Milwaukee WI 53226, USA
Beth A. McCormick
Affiliation:
Harvard University, Massachusetts
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Summary

INTRODUCTION

Bacterial pathogens utilize invasive pathways and/or toxins to subvert the innate and acquired immune systems in order to damage the host epithelium. The infectious process requires that the pathogen can adhere and proliferate in the host. The capacity to colonize and cause disease varies among bacterial pathogens. For example, Clostridium tetani has only a limited ability to bind and proliferate within the host but is pathogenic due to the production of a potent neurotoxin, but the streptococcus and staphylococcus have strong adhesion factors that allow efficient colonization, with virulence due to the production of a multitude of virulence factors, including superantigens that simultaneously bind the major histocompatibility complex (MHC) and T-cell receptor of immune cells to stimulate production of antigen-independent cytokines.

The basic distinction between a member of our normal flora and a pathogen lies in the capacity to damage the host. However, this distinction is grayed by the immune status of the host, where host compromise converts commensal bacteria or even saprophytic bacteria into potent opportunistic pathogens. Pseudomonas aeruginosa is an opportunistic pathogen in many clinical situations but does not elicit disease in healthy individuals despite its ability to produce both a classical exotoxin and type III cytotoxins. Clostridium difficile can cause pseudomembrane colitis in patients undergoing antibiotic therapy. C. difficile pathogenesis is related to the ability to produce the exotoxins, toxin A and toxin B. Escherichia coli, a component of our normal gut flora, becomes a pathogen upon the acquisition of accessory genes that can encode several classes of toxins.

Type
Chapter
Information
Bacterial-Epithelial Cell Cross-Talk
Molecular Mechanisms in Pathogenesis
, pp. 184 - 210
Publisher: Cambridge University Press
Print publication year: 2006

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