Interaction Between Chronic Endometritis Caused Endometrial Microbiota Disorder and Endometrial Immune Environment Change in Recurrent Implantation Failure

Objective To investigate the Interaction between chronic endometritis (CE) caused endometrial microbiota disorder and endometrial immune environment change in recurrent implantation failure (RIF). Method Transcriptome sequencing analysis of the endometrial of 112 patients was preform by using High-Throughput Sequencing. The endometrial microbiota of 43 patients was analyzed by using 16s rRNA sequencing technology. Result In host endometrium, CD4 T cell and macrophage exhibited significant differences abundance between CE and non-CE patients. The enrichment analysis indicated differentially expressed genes mainly enriched in immune-related functional terms. Phyllobacterium and Sphingomonas were significantly high infiltration in CE patients, and active in pathways related to carbohydrate metabolism and/or fat metabolism. The increased synthesis of lipopolysaccharide, an important immunomodulator, was the result of microbial disorders in the endometrium. Conclusion The composition of endometrial microorganisms in CE and non-CE patients were significantly different. Phyllobacterium and Sphingomonas mainly regulated immune cells by interfering with the process of carbohydrate metabolism and/or fat metabolism in the endometrium. CE endometrial microorganisms might regulate Th17 response and the ratio of Th1 to Th17 through lipopolysaccharide (LPS).

Automated summary

Investigating the interaction between chronic endometritis (CE) induced endometrial microbiota disorder and endometrial immune environment change in recurrent implantation failure (RIF), it was found that CD4 T cells and macrophages exhibited significant differences in abundance between CE and non-CE patients. The endometrial microorganisms in CE patients, particularly Phyllobacterium and Sphingomonas, played a role in regulating immune cells by interfering with carbohydrate and/or fat metabolism. The microbial disorders in CE endometrium led to increased synthesis of lipopolysaccharide, potentially affecting Th17 and Th1/Th17 ratio.