Colonic immune suppression, barrier dysfunction, and dysbiosis by gastrointestinal bacillus anthracis infection

Yaíma L. Lightfoot, Tao Yang, Bikash Sahay, Mojgan Zadeh, Sam X. Cheng, Gary P. Wang, Jennifer L. Owen, Mansour Mohamadzadeh

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

Gastrointestinal (GI) anthrax results from the ingestion of Bacillus anthracis. Herein, we investigated the pathogenesis of GI anthrax in animals orally infected with toxigenic non-encapsulated B. anthracis Sterne strain (pXO1+ pXO2-) spores that resulted in rapid animal death. B. anthracis Sterne induced significant breakdown of intestinal barrier function and led to gut dysbiosis, resulting in systemic dissemination of not only B. anthracis, but also of commensals. Disease progression significantly correlated with the deterioration of innate and T cell functions. Our studies provide critical immunologic and physiologic insights into the pathogenesis of GI anthrax infection, whereupon cleavage of mitogen-activated protein kinases (MAPKs) in immune cells may play a central role in promoting dysfunctional immune responses against this deadly pathogen. Copyright:

Original languageEnglish (US)
Article numbere100532
JournalPloS one
Volume9
Issue number6
DOIs
StatePublished - Jun 19 2014
Externally publishedYes

ASJC Scopus subject areas

  • General

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