Bacteria That Cause Enteric Diseases Stimulate Distinct Humoral Immune Responses.

Souwelimatou Amadou Amani,Mark L Lang

doi:10.3389/fimmu.2020.565648

Souwelimatou Amadou Amani, Mark L Lang

Open Access

https://doi.org/10.3389/fimmu.2020.565648

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Abstract

Bacterial enteric pathogens individually and collectively represent a serious global health burden. Humoral immune responses following natural or experimentally-induced infections are broadly appreciated to contribute to pathogen clearance and prevention of disease recurrence. Herein, we have compared observations on humoral immune mechanisms following infection with Citrobacter rodentium, the model for enteropathogenic Escherichia coli, Vibrio cholerae, Shigella species, Salmonella enterica species, and Clostridioides difficile. A comparison of what is known about the humoral immune responses to these pathogens reveals considerable variance in specific features of humoral immunity including establishment of high affinity, IgG class-switched memory B cell and long-lived plasma cell compartments. This article suggests that such variance could be contributory to persistent and recurrent disease.

Highlights

Enteric pathogens rapidly activate host innate and adaptive defense mechanisms upon infection
These mechanisms include activation of innate immune cells, their production of cytokines and chemokines, and antigen presentation necessary for the recruitment of inflammatory cells [1], and initiation of the adaptive immune response [2]. Bacteria such as Vibrio cholerae and Clostridioides difficile secrete enterotoxins that mediate the pathogenesis and the inflammatory responses which often leads to tissue injury and loss of intestinal barrier integrity. Other bacteria such as Salmonella and Shigella overcome the intestinal barrier through invasion via the microfold cells (M cells) which are specialized epithelial cells that overlie Peyer’s Patches of the intestine [3,4,5]
We present an overview of what is known about the host immune responses to five enteric pathogens: C. rodentium, V. cholerae, Shigella spp., Salmonella spp., and C

Summary

Introduction

Enteric pathogens rapidly activate host innate and adaptive defense mechanisms upon infection. Infection with C. rodentium induces a strong mucosal IgA response and systemic IgM and IgG responses specific to several antigens such as the adhesin intimin, a TTSS effector protein [34, 35]. The activation and recruitment of effector T cells requires production of SCFAs. These metabolites promote intestinal antibody responses in mice infected with C. rodentium [47, 48].

Results

Conclusion