Good girl goes bad: Understanding how gut commensals cause disease

Microb Pathog. 2024 May:190:106617. doi: 10.1016/j.micpath.2024.106617. Epub 2024 Mar 16.

Abstract

This review examines the complex connection between commensal microbiota and the development of opportunistic infections. Several underlying conditions, such as metabolic diseases and weakened immune systems, increase the vulnerability of patients to opportunistic infections. The increasing antibiotic resistance adds significant complexity to the management of infectious diseases. Although commensals have long been considered beneficial, recent research contradicts this notion by uncovering chronic illnesses linked to atypical pathogens or commensal bacteria. This review examines conditions in which commensal bacteria, which are usually beneficial, contribute to developing diseases. Commensals' support for opportunistic infections can be categorized based on factors such as colonization fitness, pathoadaptive mutation, and evasion of host immune response. Individuals with weakened immune systems are especially susceptible, highlighting the importance of mucosal host-microbiota interaction in promoting infection when conditions are inappropriate. Dysregulation of gut microbial homeostasis, immunological modulation, and microbial interactions are caused by several factors that contribute to the development of chronic illnesses. Knowledge about these mechanisms is essential for developing preventive measures, particularly for susceptible populations, and emphasizes the importance of maintaining a balanced gut microbiota in reducing the impact of opportunistic infections.

Keywords: Dysbiosis; Gut; Infection; Inflammation; Microbiota; Pathogen.

Publication types

  • Review

MeSH terms

  • Animals
  • Bacteria / classification
  • Bacteria / genetics
  • Dysbiosis
  • Gastrointestinal Microbiome*
  • Homeostasis
  • Host Microbial Interactions*
  • Humans
  • Microbial Interactions
  • Opportunistic Infections* / immunology
  • Opportunistic Infections* / microbiology
  • Symbiosis