Estrous cycle and ovariectomy-induced changes in visceral pain are microbiota-dependent

Visceral hypersensitivity (VH) is a hallmark of many functional gastrointestinal disorders including irritable bowel syndrome and is categorized by a dull, diffuse sensation of abdominal pain. Recently, the gut microbiota has been implicated in VH in male mice, but the effects in females have yet to be explored fully. To this end, we now show that somewhat surprisingly, female germ-free mice have similar visceral pain responses to colorectal distension (CRD) as their conventional controls. However, we show that although sensitivity to CRD is estrous cycle stage-dependent in conventional mice, it is not in germ-free mice. Further, ovariectomy(OVX) induced VH in conventional but not germ-free mice, and induced weight gain regardless of microbiota status. Finally, we show that estrogen-replacement ameliorated OVX-induced VH. Taken together, this study provides evidence for a major role of female sex hormones and the gut microbiota in sensation of visceral pain in females.

Automated summary

Through studying female mice, it was found that visceral hypersensitivity is closely related to sex hormones and gut microbiota; germ-free mice showed similar visceral pain responses to colorectal distension as conventional mice, with sensitivity not dependent on estrous cycle stage; ovariectomy induced hypersensitivity only in conventional mice, leading to weight gain.