Therapeutic activation of IL-22-producing innate lymphoid cells enhances host defenses to Clostridioides difficile infection.

ABSTRACT: Clostridioides difficile causes debilitating colitis via secreted toxins that disrupt the intestinal barrier, and toxemia is associated with severe disease. Thus, therapies that fortify the intestinal barrier will reduce the severity of infection. Innate lymphoid cells (ILCs) are critical in the defense against acute C. difficile infection and represent a promising therapeutic target to limit disease. Here, we report that oral administration of the Toll-like receptor (TLR) 7 agonist R848 limits intestinal damage and protects mice from lethal C. difficile infection without impacting pathogen burden or altering the intestinal microbiome. R848 induced interleukin (IL)-22 secretion by ILCs, leading to STAT3 phosphorylation in the intestinal epithelium and increased stem cell proliferation. Gen

SUBMITTER: Mears KS 

PROVIDER: S-EPMC12115236 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature