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Divergent mechanistic pathways of diarrheagenic bacterial infections at the host-microbiota interface: a review

Michael Tosin Bayode1, Oluwatoyosi Ezekiel Olawale2, Olubukola Olayemi Olusola-Makinde2

  • 1Department of Microbiology, School of Life Sciences, Federal University of Technology Akure, P.M.B 704, Akure, Ondo State, Nigeria. bayodemtmcb@futa.edu.ng.

Archives of Microbiology
|April 20, 2026
PubMed

Insights

Bacterial diarrheal diseases are a major global health burden. This review compares how pathogens like ETEC, Shigella, Salmonella, and C. difficile interact with the host and microbiota, revealing new therapeutic targets.

Area of Science:

  • Microbiology
  • Immunology
  • Gastroenterology

Background:

  • Bacterial diarrheal diseases pose significant global health challenges, especially in children in low-resource areas.
  • Key pathogens like Enterotoxigenic Escherichia coli (ETEC), Shigella, Salmonella enterica, and Clostridioides difficile cause diarrhea through distinct molecular mechanisms.
  • Understanding the complex interplay between host, pathogen, and microbiota is crucial for developing effective treatments.

Purpose of the Study:

  • To provide a comparative analysis of the pathogenicity mechanisms of major bacterial diarrheal agents.
  • To explore the role of the gut microbiota as a dynamic third player in the host-pathogen interaction.
  • To identify novel therapeutic vulnerabilities based on these mechanistic insights.

Main Methods:

  • Comparative analysis of molecular strategies employed by ETEC, Shigella, Salmonella, and C. difficile.
  • Integration of recent findings on the microbiota's role in colonization resistance and pathogen fuel provision.
  • Synthesis of advanced molecular insights, including T3SS energetics, effector-immunity interactions, and toxin receptor diversity.

Main Results:

  • Pathogenicity is defined by pathogens' unique management of host-microbiota metabolic and signaling conflicts.
  • The microbiota can either confer colonization resistance (bile acids, proline) or promote pathogen expansion (formate, tetrathionate).
  • Specific molecular mechanisms include Shigella's Spa47, OspC1/OspD3 interactions with necroptosis, Salmonella's T3SS-2 targets (LMO4, SteA), and C. difficile TcdB receptor diversity.

Conclusions:

  • Next-generation therapies should move beyond broad-spectrum antibiotics.
  • Precision bacteriophage biocontrol and AI-discovered lysins represent promising future interventions.
  • Targeting the host-microbiota-pathogen axis offers a novel therapeutic paradigm for bacterial diarrhea.

Keywords:
BacteriaDiarrheaGut microbiotaHost‒pathogen interactionVirulence factors

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