Alteration of host gut microbiota by antibiotic exposure in early life remodeled host intestinal immune development and metabolism and enhanced the induction of type 1 diabetes in genetically predisposed animals.

Nuclear receptor NHR-14 regulates the subcellular localization of the zinc transcription factor PQM-1 to coordinate innate immunity with iron sequestration during pathogen infection in C. elegans..

RNA m6A level is dually regulated during RV infection and development, METTL3 deficiency in IECs results in increased resistance to rotaviral infection through reduced m6A modificaitons on Irf7.

A mouse model of inducible inflammasome activation in intestinal epithelial cells reveals separate inflammasome-dependent and -independent cross-presentation pathways for epithelial cell-derived antigen.

Gut macrophages produce complement component C1q, which modulates neurogenic activity of gut peristalsis and is thus a key regulator of gastrointestinal motility.

Calcineurin inhibition has opposing effects on Caenorhabditis elegans lifespan and survival on pathogens via its role in the defecation motor program.

In-depth proteomic analyses of intestinal tissue-resident intraepithelial T lymphocytes reveals how these cells are adapted to the intestinal environment through increased cholesterol and lipid metabolism, tailored metabolic profiles, receptors for interacting with epithelial cells, and tightly regulated signalling pathways.

A phase transition of TIR-1/SARM1 induced by either pathogen or non-pathogen stress potentiates its intrinsic NADase activity, which activates the p38 PMK-1 signaling cascade to induce protective immune defenses in Caenorhabditis elegans intestinal epithelial cells.

In the fruit fly Drosophila melanogaster, stem cell activity ages female guts but not male guts; furthermore, males with feminized guts develop pathologies but gain an increase in lifespan through dietary restriction.

Serum amyloid A proteins bind retinol with nanomolar affinity, and do so by forming oligomers that create a hydrophobic pocket that shields retinol from the aqueous environment.