# Gut commensals require Peyer’s patches to induce protective systemic IgA responses

## TL;DR

This study shows that gut bacteria like Bacteroides fragilis can boost protective IgA antibodies in the body, with Peyer’s patches playing a key role in this immune response.

## Contribution

The study identifies Bacteroides fragilis as a strong inducer of systemic IgA and highlights the essential role of Peyer’s patches in this process.

## Key findings

- Bacteroides fragilis induces high levels of systemic IgA in a colonization-dependent manner.
- Peyer’s patches are crucial for Bacteroides fragilis-induced IgA responses, while cecal patches are not.
- Bacteroides fragilis colonization protects mice from peritoneal abscess formation in a bowel perforation model.

## Abstract

Gut educated IgA secreting plasma cells that disseminate beyond the mucosa and into systemic tissues have been described as providing beneficial effects from disease in several contexts. Several bacteria have been implicated in the induction of systemic IgA, however the mechanisms that result in differential levels of induction by each bacterial species are still unknown. Here we show, the commensal bacteria, Bacteroides fragilis (Bf), is an efficient inducer of systemic IgA responses. The ability of Bf to induce the production of bone marrow IgA plasma cells and high levels of serum IgA relied on high levels of gut colonization in a dose-dependent manner. Colonization induced Bf-specific IgA responses were severely diminished in the absence of Peyer’s patches, but not the murine cecal patch. Colonization of mice with Bf, a natural human commensal, resulted in few changes within the microbiome and the host transcriptional profile in the gut, suggesting a commensal relationship with the host. Bf colonization did benefit the mice by inducing systemic IgA that led to increased protection in a bowel perforation model resulting in lower peritoneal abscess formation. These findings demonstrate a critical role for bacterial colonization and Peyer’s patches in the induction of robust systemic IgA responses that confer protection from bacterial dissemination outside of the gut.