| First Author | Wu J | Year | 2025 |
| Journal | Cell Host Microbe | Volume | 33 |
| Issue | 1 | Pages | 119-136.e11 |
| PubMed ID | 39788092 | Mgi Jnum | J:363676 |
| Mgi Id | MGI:7856358 | Doi | 10.1016/j.chom.2024.12.006 |
| Citation | Wu J, et al. (2025) The intestinal fungus Aspergillus tubingensis promotes polycystic ovary syndrome through a secondary metabolite. Cell Host Microbe 33(1):119-136.e11 |
| abstractText | Polycystic ovary syndrome (PCOS) affects 6%-10% of women of reproductive age and is known to be associated with disruptions in the gut bacteria. However, the role of the gut mycobiota in PCOS pathology remains unclear. Using culture-dependent and internal transcribed spacer 2 (ITS2)-sequencing methods, we discovered an enrichment of the gut-colonizable fungus Aspergillus tubingensis in 226 individuals, with or without PCOS, from 3 different geographical areas within China. Colonization of mice with A. tubingensis led to a PCOS-like phenotype due to inhibition of Aryl hydrocarbon receptor (AhR) signaling and reduced interleukin (IL)-22 secretion in intestinal group 3 innate lymphoid cells (ILC3s). By developing a strain-diversity-based-activity metabolite screening workflow, we identified secondary metabolite AT-C1 as an endogenous AhR antagonist and a key mediator of PCOS. Our findings demonstrate that an intestinal fungus and its secondary metabolite play a critical role in PCOS pathogenesis, offering a therapeutic strategy for improving the management of the disease. |
