Evidence map›Paper›PMID 41586117›Full record

ArticleJournal of reproduction & infertility

Altered Expression of Toll-Like Receptors and Key Signaling Genes in Sertoli Cells of Azoospermic Patients.

Mohammad Reza Lakpour, Reza Aflatoonian, Mohammad Ali Sadighi Gilani, Reza Hajihosseini, Marjan Sabbaghian

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Article in Journal of reproduction & infertility. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

5 authors.

Mohammad Reza LakpourDepartment of Biology, Payame Noor University, Tehran, Iran.
Reza AflatoonianDepartment of Endocrinology and Female Infertility, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
Mohammad Ali Sadighi GilaniDepartment of Andrology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
Reza HajihosseiniDepartment of Biology, Payame Noor University, Tehran, Iran.
Marjan SabbaghianDepartment of Andrology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Azoospermia, the complete absence of sperm in the ejaculate, is a major cause of male infertility. Sertoli cells are essential for spermatogenesis, and disruptions in innate immune immune pathways, particularly Toll-like receptors (TLRs), may impair their function. This study investigated the expression of TLR1-10 and downstream signaling molecules (MYD88, NFKB, TRIF, IRF3, and TRAM) in Sertoli cells of azoospermic patients. Methods: Testicular tissue were collected from 20 azoospermic men undergoing testicular sperm extraction (TESE). Patients were categorized into two TESE positive (sperm present, n=10) and TESE negative (sperm absent, n=10). Sertoli cells were isolated using enzyme digestion and purified via fluorescence-activated cell sorting (FACS). Gene expression of TLR1-10 and signaling molecules was quantified by RTPCR. Data were analyzed using independent-samples T-test, with significance set at p< 0.05. Results: Significant downregulation was detected in TLR10 (20.6-fold, p<0.0001), TLR9 (4.6-fold, p<0.05), TLR7 (4.8-fold, p<0.01), TLR6 (12.4-fold, p<0.05), TLR5 (13.5-fold, p<0.001), TLR4 (3.2-fold, p<0.05), and TLR3 (3.1-fold, p<0.01). Among signaling molecules, MYD88 (4.1-fold, p<0.01) and IRF3 (4.2-fold, p<0.05) showed significant reductions, indicating impaired immune signaling in Sertoli cells of TESE-negative men. Conclusion: Altered expression of TLRs and associated signaling molecules in Sertoli cells of azoospermic men suggests innate immune dysregulation as a potential mechanism underlying defective spermatogenesis. These findings highlight immune privilege-associated pathways as possible targets for developing diagnostic biomarkers and novel therapeutic approaches for male infertility.

Indexed as

AzoospermiaMale infertilitySertoli cellsSignaling transductionTESEToll-like receptors

Identifiers

PMID41586117
PMCPMC12828058

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