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The Gut-Origin Septic States

  • J. R. Border
Conference paper

Abstract

The gut contains sufficient bacteria and toxins to kill the host millions of times over. In normal life these toxic entities are confined to the gut by processes dependent upon food ingestion, defecation, the interactions of the gut associated lymphoid tissue and the systemic immune system, and the function of various valves such as the glottis and gastro esophageal junction. Food ingestion stimulates salivary gland secretion, stomach digestion, biliary tract secretions, replication of enterocytes, mucous secretion, and growth of commensal bacteria. Secretory IgA is delivered to the lumen of the gut by the salivary gland, biliary tract secretions and in mucous. Secretory IgA binds to bacteria and thus prevents binding of the bacteria to the enterocyte in preparation for penetration. The gut mucosa wall is continually renewed by a process of cell and mucous shedding which also aids in preventing bacterial binding and penetration. Finally, commensal bacteria bind to the enterocytes where they consume available nutrients, prevent pathogenic bacteria binding, and release metabolites toxic to pathogenic bacteria. It is the growth of commensal bacteria that is the primary factor that prevents growth of pathogenic bacteria in the gut.

Keywords

Injury Severity Score Positive Blood Culture Commensal Bacterium Septic State Original Injury 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag, Berlin Heidelberg 1989

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  • J. R. Border

There are no affiliations available

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