Abstract

The intestinal microbiota is a large and diverse microbial community that inhabits the intestine, containing about 100 trillion bacteria of 500-1000 distinct species that, collectively, provide benefits to the host. The human gut microbiota composition is determined by a myriad of factors, among them genetic and environmental, including diet and medication. The microbiota contributes to nutrient absorption and maturation of the immune system. As reciprocity, the host immune system plays a central role in shaping the composition and localization of the intestinal microbiota. Secretory immunoglobulins A (sIgAs), component of the adaptive immune system, are important player in the protection of epithelium, and are known to have an important impact on the regulation of microbiota composition. A recent study published in Immunity by Fransen and colleagues aimed to mechanistically decipher the interrelationship between sIgA and microbiota diversity/composition. This commentary will discuss these important new findings, as well as how future therapies can ultimately benefit from such discovery.

Highlights

  • The gut host defense system comprises an array of mechanisms to keep the microbiota in check, maintaining an orderly beneficial relationship with the intestinal microbiota [1]

  • We will discuss recent findings describing how Immunoglobulin A (IgA) population has an impact on microbiota diversity, and how they may provide therapeutic insights into diseases associated with dysbiosis [2]

  • This study demonstrates that transfer of a microbiota from an IgA-low mice, by co-housing or fecal transplantation, can lower fecal IgA levels in IgAhigh mice [17]

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Summary

Introduction

The gut host defense system comprises an array of mechanisms to keep the microbiota in check, maintaining an orderly beneficial relationship with the intestinal microbiota [1]. One of the main role played by IgA is the promotion of immune exclusion by entrapping dietary antigens and microorganisms in the mucus, or down-regulating the expression of pro-inflammatory bacterial epitopes on commensal bacteria, such as flagellin [6].

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