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Bacterial Toxin Leads To Systemic Infection

Apr. 2, 2009 — A group led by Dr. Michael Klapproth at Emory University, Atlanta suggests that bacterial lymphotoxin disrupts intestinal epithelial barrier function.


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They report these findings in the April 2009 issue of The American Journal of Pathology.

Numerous bacterial species commonly live in the human gut. These bacteria contribute to digestion, but also may cause disease. Some bacteria, such as Escheria coli (E. coli) or Citrobacter rodentium (C. rodentium), can breach the intestinal epithelial barrier, entering the blood and causing systemic infection.

Lymphostatin, a toxin produced by gram negative bacteria including E. coli and C. rodentium, has been associated with bacterial virulence. To determine if lymphostatin affects epithelial barrier integrity, Babbin et al generated two strains of C. rodentium, CrGIM21 and CrPrM5, with different mutations in lymphostatin. Whereas wild-type C. rodentium disrupted epithelial barrier function, CrGIM21 and CrPrM5 had reduced effects on two aspects of epithelial cell function. These data suggest that lymphostatin may be a strong target candidate for treatment of enteric gram negative bacteria.

Dr. Klapporth and colleagues postulate that "therapeutic interventions in form of specific immunoglobulins directed against lymphostatin and its enzymatic activities might provide an attractive alternative to antibiotics in treating intestinal injury and preventing extraintestinal manifestations of Gram negative infection."

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The above story is reprinted from materials provided by American Journal of Pathology, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Babbin BA, Sasaki M, Gerner-Schmidt KW, Nusrat A, Klapproth J-M A. The Bacterial Virulence Factor Lymphostatin Compromises Intestinal Epithelial Barrier Function by Modulating Rho GTPases. American Journal Of Pathology, 2009; DOI: 10.2353/ajpath.2009.080640
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