Chlamydia trachomatis infection regulates the expression of tetraspanins, activin-A, and inhibin-A in tubal ectopic pregnancy

Abstract

Mechanism of Chlamydia trachomatis causing tubal ectopic pregnancy (EP) is not well understood. Tetraspanins (tspans), activin-A and inhibin-A might play role in development of pathological conditions leading to EP. The study aimed to elucidate the expression of tspans, activin-A and inhibin-A with role of associated cytokines in C. trachomatis-associated EP and analyze interacting partners of DEGs, with expression of few important interacting genes. Fallopian tissue and serum were collected from 100 EP (Group I) and 100 controls (Group II) from SJH, New Delhi, India. Detection of C. trachomatis was done by PCR and IgG antibodies were detected by ELISA. Expression of tspans, activin-A and inhibin-A and cytokines was analyzed by RT-PCR and their interacting genes was assessed by STRING. Expression of few disease-associated interacting genes was studied by RT-PCR. 29% (Group I) were C. trachomatis positive. Tspans and activin-A were significantly upregulated while inhibin-A was significantly downregulated in Group Ia. ITGA1, TLR-2, ITGB2, Smad-3 were few interacting genes. Expression of ITGA1, TLR-2 and Smad-3 was significantly upregulated in C. trachomatis positive-EP. Results suggested dysregulated tspans, activin-A and inhibin-A might play role in C. trachomatis-infected tubal EP.

Morphology of the immune cells in the wall of the human uterine tube and their possible impact on reproduction—uterine tube as a possible immune privileged organ

“…The uterine tube, as well as other parts of the upper female reproductive system, is immunologically unique in its requirements for tolerance to allogenic sperm and semi-allogenic embryos, yet responds to an array of sexually transmitted pathogens. Although uterine tubes are considered sterile, microorganisms can ascend from the lower reproductive tract, causing pelvic inflammatory disease and/or reproductive alterations such as ectopic pregnancy ( Caven and Carabeo, 2023 ; Jenabi et al, 2023 ; Pant et al, 2023 ) and tubal infertility ( Hoenderboom et al, 2019 ; Liu et al, 2022 ). In general, uterine tube diseases account for 25%–35% of female factor infertility.…”