Nejvíce citovaný článek - PubMed ID 29174402
Closely related host species share similar symbionts, but the effects of host genetic admixture and environmental conditions on these communities remain largely unknown. We investigated the influence of host genetic admixture and environmental factors on the intestinal prokaryotic and eukaryotic communities (fungi, parasites) of two house mouse subspecies (Mus musculus domesticus and M. m. musculus) and their hybrids in two settings: (i) wild-caught mice from the European hybrid zone and (ii) wild-derived inbred mice in a controlled laboratory environment before and during a community perturbation (infection). In wild-caught mice, environmental factors strongly predicted the overall microbiome composition. Subspecies' genetic distance significantly influenced the overall microbiome composition, and each component (bacteria, parasites and fungi). While hybridization had a weak effect, it significantly impacted fungal composition. We observed similar patterns in wild-derived mice, where genetic distances and hybridization influenced microbiome composition, with fungi being more stable to infection-induced perturbations than other microbiome components. Subspecies' genetic distance has a stronger and consistent effect across microbiome components than differences in expected heterozygosity among hybrids, suggesting that host divergence and host filtering play a key role in microbiome divergence, influenced by environmental factors. Our findings offer new insights into the eco-evolutionary processes shaping host-microbiome interactions.
- Klíčová slova
- host–microbiome interactions, hybridization, microbiome, spatial environment, species barriers,
- MeSH
- biologická evoluce MeSH
- hybridizace genetická * MeSH
- interakce mikroorganismu a hostitele MeSH
- mikrobiota MeSH
- myši MeSH
- střevní mikroflóra MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Patients with loss of function in the gene encoding the master regulator of central tolerance AIRE suffer from a devastating disorder called autoimmune polyendocrine syndrome type 1 (APS-1), characterized by a spectrum of autoimmune diseases and severe mucocutaneous candidiasis. Although the key mechanisms underlying the development of autoimmunity in patients with APS-1 are well established, the underlying cause of the increased susceptibility to Candida albicans infection remains less understood. Here, we show that Aire+MHCII+ type 3 innate lymphoid cells (ILC3s) could sense, internalize and present C. albicans and had a critical role in the induction of Candida-specific T helper 17 (TH17) cell clones. Extrathymic Rorc-Cre-mediated deletion of Aire resulted in impaired generation of Candida-specific TH17 cells and subsequent overgrowth of C. albicans in the mucosal tissues. Collectively, our observations identify a previously unrecognized regulatory mechanism for effective defense responses against fungal infections.
