# Impact of Gastrointestinal Bacillus anthracis Infection on Hepatic B Cells

## TL;DR

This study explores how a gastrointestinal Bacillus anthracis infection affects B cells in the liver and may lead to systemic bacterial spread.

## Contribution

The study reveals that GI anthrax causes migration of specific B cells to the liver, potentially to combat systemic infection.

## Key findings

- Bacillus anthracis and gut bacteria migrate to the liver during GI anthrax.
- B-1a and MZ-like B cells increase in the liver despite a global B cell population decline.
- Increased chemokine expression is observed with the accumulation of these B cells in the liver.

## Abstract

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.