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Microbiota-derived acetate protects against UPEC-epididymo-orchitis by improving the phagocytosis of testicular macrophages.

ABSTRACT: The gut microbiota is intimately associated with maintaining a stable intestinal immune balance. However, it remains unclear whether gut dysbiosis affects the homeostasis within the testes. In our DSS-induced colitis mouse model, we observed increased inflammatory cell infiltration within the mouse testes. Analysis of the gut microbiota in the feces of DSS colitis mice and mice treated with antibiotics revealed a significant decrease in the number of bacteria related to cellulose decomposition in the gut, as well as a decrease in the content of short-chain fatty acid salts in the peripheral blood of mice. In vitro experiments found that acetate can significantly improve the outcome of UPEC-induced bacterial epididymo-orchitis. Further in vitro experiments demonstrated that acetate can enhance the bacterial phagocytic ability of testicular macrophages (TM), accelerate the early clearance of bacteria within the testes, and thus reduce the degree of testicular inflammation. This study provides a link to explain the progression of bacterial epididymo-orchitis in relation to gut microbiota dysbiosis and offers new insights for the treatment of bacterial epididymo-orchitis.

ORGANISM(S): Mus musculus

PROVIDER: GSE281537 | GEO | 2025/05/01

REPOSITORIES: GEO

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Project description:Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as CrohnM-bM-^@M-^Ys disease and colorectal cancer. Here, we show that dysbiosis coupled to Nod2 or Rip2 deficiency suffices to cause an increased risk for intestinal inflammation and colitis-associated carcinogenesis in mice. Aggravated epithelial lesions and dysplasia upon chemical-induced injury associated with loss of Nod2 or Rip2 can be prevented by antibiotics or anti-IL6R treatment. Nod2-mediated risk for intestinal inflammation and colitis-associated tumorigenesis is communicable through maternally-transmitted microbiota even to wild-type hosts. Disease progression was identified to drive complex NOD2-dependent changes of the colonic-associated microbiota. Reciprocal microbiota transplantation rescues the vulnerability of Nod2-deficient mice to colonic injury. Altogether, our results unveil an unexpected function for NOD2 in shaping a protective assembly of gut microbial communities, providing a rationale for intentional manipulation of genotype-dependent dysbiosis as a causative therapeutic principle in chronic intestinal inflammation. Analysis used RNA extracted from colonic mucosa of untreated, antibiotics-treated or metronidazole-treated C57Bl/6J and Nod2-deficient mice in CAC model. Direct comparisons were performed as follow: C57Bl/6J untreated mice vs Nod2-deficient untreated mice, C57Bl/6J antibiotics-treated mice vs Nod2-deficient antibiotics-treated mice, C57Bl/6J metronidazole-treated mice vs Nod2-deficient metronidazole-treated mice, C57Bl/6J untreated mice vs C57Bl/6J antibiotics-treated mice, C57Bl/6J untreated mice vs C57Bl/6J metronidazole-treated mice, Nod2-deficient untreated mice vs Nod2-deficient antibiotics-treated mice, Nod2-deficient untreated mice vs Nod2-deficient metronidazole-treated mice. Indirect comparisons with control data were made across multiple arrays with raw data pulled from different channels for data analysis.

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Microbiota-derived acetate protects against UPEC-epididymo-orchitis by improving the phagocytosis of testicular macrophages.

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