Impact of Gastrointestinal Bacillus anthracis Infection on Hepatic B Cells

Toxins

Natacha Colliou²  Bikash Sahay²  Mojgan Zadeh²  Jennifer L. Owen¹  Mansour Mohamadzadeh² 

[1] Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610, USA; E-Mail:;Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA; E-Mails:

关键词: B cells;    gastrointestinal anthrax;    innate lymphoid cells;    liver;   

DOI  :  10.3390/toxins7093805

来源: mdpi

【 摘 要 】

Ingestion of Bacillus anthracis results in rapid gastrointestinal (GI) infection, known as GI anthrax. We previously showed that during GI anthrax, there is swift deterioration of intestinal barrier function leading to translocation of gut-associated bacteria into systemic circulation. Additionally, we described dysfunction in colonic B cells. In concordance with our previous studies, here, we report early migration of the Sterne strain of B. anthracis along with other gut-resident bacteria into the infected murine liver. Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells. Both of these cell types are capable of producing immunoglobulins against common pathogens and commensals, which act as a general antibody barrier before an antigen-specific antibody response. Accumulation of these cells in the liver was associated with an increase in chemokine expression. These data suggest that the presence of Sterne and other commensals in the liver trigger migration of MZ-like B cells from the spleen to the liver to neutralize systemic spread. Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.