ATG16L1 in myeloid cells limits colorectal tumor growth in Apc^Min/+ mice infected with colibactin-producing Escherichia coli via decreasing inflammasome activation.

ABSTRACT: Escherichia coli strains producing the genotoxin colibactin, designated as CoPEC (colibactin-producing E. coli), have emerged as an important player in the etiology of colorectal cancer (CRC). Here, we investigated the role of macroautophagy/autophagy in myeloid cells, an important component of the tumor microenvironment, in the tumorigenesis of a susceptible mouse model infected with CoPEC. For that, a preclinical mouse model of CRC, the Apc^Min/+ mice, with Atg16l1 deficiency specifically in myeloid cells (Apc^Min/+/Atg16l1[∆MC]) and the corresponding control mice (Apc^Min/+), were infected with a clinical CoPEC strain 11G5 or its isogenic mutant 11G5∆clbQ that does not produce coli

SUBMITTER: Salesse L 

PROVIDER: S-EPMC11423662 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature