AI Insight
This study investigated type 6 secretion systems (T6SS) in adherent-invasive Escherichia coli (AIEC) bacteria found in Crohn's disease patients. Researchers found that T6SS genes are more common in the gut microbiota of Crohn's disease patients compared to healthy individuals, and that these molecular systems are activated by gastrointestinal conditions, particularly bile salts. Mouse experiments demonstrated that T6SS enable AIEC bacteria to alter the composition of gut microbiota attached to intestinal mucosa, suggesting these systems help pathogenic bacteria compete with normal gut bacteria to establish colonization.
Why it matters
Understanding how AIEC bacteria use T6SS to outcompete beneficial gut microbiota could lead to new therapeutic strategies for Crohn's disease. Targeting these secretion systems might prevent pathogenic bacterial colonization and help restore healthy microbial balance in patients with inflammatory bowel disease.
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⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Adherent Invasive Escherichia coli (AIEC) colonize the ileal mucosa of Crohn’s disease patients. Among bacterial virulence factors potentially implicated, type 6 secretion systems (T6SS) are molecular machineries sending effectors in prokaryotic or eukaryotic target cells. Two T6SS have been reported in AIEC LF82 reference strain. Here, we show that T6SS genes are more prevalent in Crohn’s disease patients’ microbiota compared to healthy controls, and that T6SS are more frequent in AIEC pathovar compared to E. coli in general and associated with FimH pathoadaptive polymorphism. The use of an in vitro gastrointestinal system coupled with T6SS promoter reporter assay highlighted expression of LF82 T6SS under gastrointestinal conditions, with a major role for bile salts. In mice infected with AIEC LF82 versus T6SS-deleted mutants, T6SS showed a functional impact in modulating the composition of mucosa-associated gut microbiota. Thus, AIEC may use their T6SS to compete with endogenous microbiota to colonize host mucosa.