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Updated: Apr 4, 2026

Flow Cytometric Analysis of Biomarkers for Detecting Human Sperm Functional Defects
Published on: April 21, 2022
CLINICAL AND ANAMNESTIC CHARACTERISTICS OF DEVELOPMENT OF ANTISPERM IMMUNITY IN INFERTILE MEN
1D. Tvildiani Medical University, Tbilisi; I. Javakhishvili Tbilisi State University, Medical Faculty; National Centre of Dermatology and Venerology, Tbilisi, Georgia.
Certain sexually transmitted infections and testicular pathologies significantly increase antisperm antibodies (ASAs), contributing to autoimmune infertility. These factors disrupt the blood-testicular barrier, damaging sperm production.
Area of Science:
- Reproductive Immunology
- Andrology
- Infectious Diseases
Background:
- Antisperm antibodies (ASAs) are implicated in male infertility.
- The specific etiological factors contributing to ASA development require further elucidation.
Purpose of the Study:
- To investigate the association between infertility duration, patient age, and various pathologies with antisperm antibody (ASA) pathogenesis.
- To identify specific infections and conditions that significantly influence ASA levels.
Main Methods:
- Retrospective analysis of 496 outpatient records.
- Inclusion criteria: infertility ≥18 months, high ASA concentration in blood and sperm.
- Evaluation of anamnestic data and clinico-laboratory test results.
Main Results:
- No significant correlation found between ASAs and general illnesses, profession, family history, autoimmune diseases, or extragenital pathologies.
- Chlamydia trachomatis, Ureaplasma urealyticum, and Mycoplasma hominis significantly increased ASA levels in blood and ejaculate (p<0.001).
- Orchitis and epididymitis showed a statistically insignificant increase in ASAs, but play a role in antisperm immunity development.
Conclusions:
- Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis, orchitis, and epididymitis contribute to ASA development.
- These conditions likely cause blood-testicular barrier dysfunction, leading to spermatogenic epithelium damage and autoimmune infertility.
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