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There is a growing body of evidence which suggests that intestinal microbiota, especially  Fusobacterium nucleatum  ( F. nucleatum ), are associated with intestinal immune disease such as ulcerative colitis (UC). The mechanism by which  F. nucleatum  promotes intestinal epithelial cell (IEC) death remained undefined. Here, we investigated the potential mechanisms about how  F. nucleatum  aggravates IEC death in UC. We first detected the abundance of  F. nucleatum  in UC tissues and analyzed its relationship with the clinical characteristics of UC. Next, we explored whether  F. nucleatum  promotes intestinal epithelial cell death  in vitro  and  in vivo . Furthermore, we extracted lipopolysaccharide (LPS) of the  F. nucleatum  and examined whether  F. nucleatum  exacerbates UC  via  LPS. Our results indicated that  F. nucleatum  was abundant in UC tissues and was correlated with clinical characteristics. In addition, we demonstrated that  F. nucleatum  and its LPS aggravated IEC death by promoted IEC autophagy. Furthermore, autophagy inhibitors, chloroquine (CQ), 3-methyladenine (3-MA) or Atg5 silencing prevented IEC death mediated by  F. nucleatum , which suggests  F. nucleatum  may contribute to UC by activating autophagic cell death. All our results uncover a vital role of  F. nucleatum  in autophagic cell death and UC, giving rise to a new sight for UC therapy by inhibiting excessive IEC autophagy and autophagic cell death.

Fusobacterium nucleatum Promotes the Development of Ulcerative Colitis by Inducing the Autophagic Cell Death of Intestinal Epithelial