From a hunger-regulating hormone to an antimicrobial peptide: gastrointestinal derived circulating endocrine hormone-peptide YY exerts exocrine antimicrobial effects against selective gut microbiota

Figures & data

Figure 1. Mechanism of PYY release from paneth cells (PCs), its regulation by fungal symbionts, and their potential implications in inflammatory bowel disease.

(a) In a healthy ileum, symbiotic yeast does not stimulate the release of PYY_1–36 from PCs. Increased virulent hyphae (blue hyphae) trigger the release of PYY_1–36 from PCs into the mucus. PYY_1–36 then targets and eliminates the hyphae (red hyphae), thereby modulating the fungal communities in the gut. (b) In inflammatory bowel disease, such as iCD, elevated mycelial load contributes to immune activation and inflammation. PC dysfunction (represented by brown PCs), is accompanied by a decrease in PYY_1–36 release or mucus depletion.

Figure 2. The gut-brain hormone axis: bidirectional hormone signaling between the gut and central nervous system.

The gastrointestinal tract secretes multiple types of peptide hormones into the circulatory system, which pass the blood brain barrier and regulate multiple neuroendocrine circuits in the central nervous system, particularly the hypothalamic region to modulate appetite and eating behavior. AgRP, agouti gene-related protein; ARC, arcuate nucleus; CCK, cholecystokinin; CNS, central nervous system; EECs, enteroendocrine cells; ENS, enteric nervous system; GLP-1, glucagon-like peptide-1; IECs, intestinal epithelial cells; NPY, neuropeptide Y; POMC, proopiomelanocortin; PVN, paraventricular nucleus; PYY, peptide YY.

Data availability statement

All of the data generated from this article are all included in this manuscript.