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Anthrax lethal toxin disrupts intestinal barrier function and causes systemic infections with enteric bacteria

Chen Sun1, Hui Fang, Tao Xie

  • 1Laboratory of Cell Biology, Division of Monoclonal Antibodies, Office of Biotechnology Products, Center for Drug Evaluation and Research, United States Food and Drug Administration, Bethesda, Maryland, United States of America.

Plos One
|March 23, 2012
PubMed

Insights

Bacillus anthracis lethal toxin (LT) disrupts intestinal barrier integrity by targeting mitogen-activated protein kinase (MAPK) pathways. This compromises the gut's defenses, potentially enabling systemic infection.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Intestinal pathogens often target host signaling pathways like mitogen-activated protein kinase (MAPK).
  • Bacillus anthracis utilizes lethal toxin (LT) to interfere with MAPK signaling by cleaving MAPK kinases (MKKs).

Purpose of the Study:

  • To investigate the effects of anthrax lethal toxin (LT) on intestinal epithelial integrity and barrier function.
  • To elucidate the role of LT's proteolytic activity in intestinal pathology and systemic infection.

Main Methods:

  • Intoxication of C57BL/6J mice with varying doses of intravenous LT.
  • Assessment of intestinal epithelial integrity, crypt cell proliferation, and apoptosis.
  • Evaluation of systemic infection development and the impact of antibiotics.

Main Results:

  • LT caused dose-dependent intestinal erosion, ulceration, and bleeding.
  • LT blocked intestinal crypt cell proliferation and induced apoptosis in villus tips.
  • Intravenous LT administration led to systemic infections with enteric organisms within 72 hours.
  • Antibiotics partially attenuated LT-induced intestinal pathology, suggesting a dual role in infection.

Conclusions:

  • Anthrax LT compromises intestinal barrier integrity by targeting MAPK pathways, weakening mucosal defenses.
  • Disruption of the intestinal barrier, coupled with LT's immunosuppressive effects, facilitates host invasion via the enteric route.
  • These findings offer a mechanism for Bacillus anthracis pathogenesis during natural infection.

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