The microbial genotoxin colibactin exacerbates mismatch repair mutations in colorectal tumors.

Certain Enterobacteriaceae strains contain a 54-kb biosynthetic gene cluster referred to as "pks" encoding the biosynthesis of a secondary metabolite, colibactin. Colibactin-producing E. coli promote colorectal cancer (CRC) in preclinical models, and in vitro induce a specific mutational signature that is also detected in human CRC genomes.

The aryl hydrocarbon receptor cell intrinsically promotes resident memory CD8 T cell differentiation and function.

The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4 T cells; however, its cell-intrinsic role in CD8 T cells remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8 T cell (T) differentiation and function. Genetic ablation of Ahr in mouse CD8 T cells leads to increased CD127KLRG1 short-lived effector cells and CD44CD62L T central memory cells but reduced granzyme-B-producing CD69CD103 T cells.

Microbial host interactions in IBD: implications for pathogenesis and therapy.

Crohn's disease (CD), ulcerative colitis (UC), and pouchitis appear to be caused by pathogenic T-cell responses to discrete antigens from the complex luminal microbiota, with susceptibility conferred by genetic polymorphisms that regulate bacterial killing, mucosal barrier function, or immune responses. Environmental triggers initiate or reactivate inflammation and modulate genetic susceptibility. New pathogenesis concepts include defective bacterial killing by innate immune cells in CD, colonization of the ileum in CD with functionally abnormal Escherichia coli that adhere to and invade epithelial cells and resist bacterial killing, and alterations in enteric microbiota composition in CD, UC, and pouchitis detected by molecular probes.