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Review

Neglected gut microbiome: interactions of the non-bacterial gut microbiota with enteric pathogens

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Article: 2226916 | Received 24 Mar 2023, Accepted 14 Jun 2023, Published online: 26 Jun 2023
 

ABSTRACT

A diverse array of commensal microorganisms inhabits the human intestinal tract. The most abundant and most studied members of this microbial community are undoubtedly bacteria. Their important role in gut physiology, defense against pathogens, and immune system education has been well documented over the last decades. However, the gut microbiome is not restricted to bacteria. It encompasses the entire breadth of microbial life: viruses, archaea, fungi, protists, and parasitic worms can also be found in the gut. While less studied than bacteria, their divergent but important roles during health and disease have become increasingly more appreciated. This review focuses on these understudied members of the gut microbiome. We will detail the composition and development of these microbial communities and will specifically highlight their functional interactions with enteric pathogens, such as species of the family Enterobacteriaceae. The interactions can be direct through physical interactions, or indirect through secreted metabolites or modulation of the immune response. We will present general concepts and specific examples of how non-bacterial gut communities modulate bacterial pathogenesis and present an outlook for future gut microbiome research that includes these communities.

This article is part of the following collections:
Enteric Bacterial Infections

Acknowledgments

We want to thank all lab members for critical reading of the manuscript. Figures were created at Biorender.com.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by a grant from the National Institute of Health to J.B. (AI143641-01) and by startup funds from the Department of Microbiology and Immunology at the University of Illinois Chicago. O.A.T. was additionally supported by training grant T32HL007829..