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Contribution of Toxin-Antitoxin Systems to Adherent-Invasive E. coli Pathogenesis.
Bustamante, Paula; Ramos-Corominas, María Núria; Martinez-Medina, Margarita.
Afiliação
  • Bustamante P; Molecular and Cellular Microbiology Laboratory, Instituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Santiago 8910060, Chile.
  • Ramos-Corominas MN; Microbiology of Intestinal Diseases, Biology Department, Universitat de Girona, 17003 Girona, Spain.
  • Martinez-Medina M; Microbiology of Intestinal Diseases, Biology Department, Universitat de Girona, 17003 Girona, Spain.
Microorganisms ; 12(6)2024 Jun 06.
Article em En | MEDLINE | ID: mdl-38930540
ABSTRACT
Pathobionts have been implicated in various chronic diseases, including Crohn's disease (CD), a multifactorial chronic inflammatory condition that primarily affects the gastrointestinal tract, causing inflammation and damage to the digestive system. While the exact cause of CD remains unclear, adherent-invasive Escherichia coli (AIEC) strains have emerged as key contributors to its pathogenesis. AIEC are characterized by their ability to adhere to and invade intestinal epithelial cells and survive and replicate inside macrophages. However, the mechanisms underlying the virulence and persistence of AIEC within their host remain the subject of intensive research. Toxin-antitoxin systems (TAs) play a potential role in AIEC pathogenesis and may be therapeutic targets. These systems generally consist of two components a toxin harmful to the cell and an antitoxin that neutralizes the toxin's effects. They contribute to bacterial survival in adverse conditions and regulate bacterial growth and behavior, affecting various cellular processes in bacterial pathogens. This review focuses on the current information available to determine the roles of TAs in the pathogenicity of AIEC. Their contribution to the AIEC stress response, biofilm formation, phage inhibition, the maintenance of mobile genetic elements, and host lifestyles is discussed.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Microorganisms Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Microorganisms Ano de publicação: 2024 Tipo de documento: Article