The peptidoglycan as a signalling molecule in the host
Event details
| Date | 07.07.2015 |
| Hour | 17:00 › 18:00 |
| Speaker | Ivo Boneca - Institut Pasteur - Unité Biologie et génétique de la paroi bactérienne - Paris - France |
| Location | |
| Category | Conferences - Seminars |
The intestinal bacterial flora plays a critical role in human health and disease; host recognition of bacterial components, such as peptidoglycan (PGN), triggers maturation of host physiology and modulates immune homeostasis. PGN is sensed by intracellular NOD-like receptors NOD1 and NOD2, and can promote or suppress the gut inflammatory response. PGN released by gut microbiota can cross the intestinal epithelial barrier and disseminate systemically in the host to mediate immune homeostasis, however PGN transcytosis pathways and the subsequent interactions with the host innate immune system upon reaching the immunologically rich niche of the intestinal lamina propria have not been characterised. Using fluorescent PGN molecules as probes to trace PGN uptake in the mouse gut, we found that PGN accumulates in lamina propria eosinophils – a completely unanticipated role for these granulocytes. This observation is compelling, as in mammals the gut is the major tissue niche for eosinophils, yet the reason for their abundance in the gut at the steady state is largely unknown. We show that transcytosis of the epithelial barrier and uptake of PGN by eosinophils is an extremely rapid processes. We then used quantitative multi-analyte profiling to assess the host response to orally administered PGN in an axenic (germ-free) mouse model. We found that key eosinophil and monocyte recruitment factors are induced in response to PGN. Our data therefore indicates a prominent role for eosinophils in regulation of gut immune homeostasis in response to PGN. Our continuing work aims to decipher how PGN signalling modulates host gut physiology and the role of eosinophils in this context.
Practical information
- General public
- Free
Organizer
- Bruno Lemaitre