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Surfactant protein D regulates murine testicular immune milieu and sperm functions
Author(s) -
Rokade Sushama,
Kishore Uday,
Madan Taruna
Publication year - 2017
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12629
Subject(s) - immune system , biology , sperm , immune privilege , endocrinology , inflammation , spermatogenesis , medicine , sperm motility , lipopolysaccharide , andrology , capacitation , immunology , botany
Problem Surfactant protein D ( SP ‐D), a pattern recognition protein that regulates inflammation and immune homoeostasis, is expressed by testicular germ cells under the influence of testosterone. This study investigates the role of SP ‐D in testicular immune privilege and sperm functions. Method of study Testicular levels of cytokines and immunoregulatory molecules were evaluated in lipopolysaccharide ( LPS )‐challenged SP ‐D gene knockout mice ( SP ‐D −/− ). Further, sperm functions were assessed by computer‐assisted sperm analyser ( CASA ) and in vitro capacitation. The effect of a recombinant fragment of human SP ‐D (rh SP ‐D) on LPS ‐induced testicular inflammation and sperm motility was assessed in wild‐type ( WT ) mice. Result Endogenous absence of SP ‐D led to significantly increased testicular levels of immunosuppressive molecules, viz. serpina3, TGF ‐β1 and IL ‐10, and reduced levels of immune cell activation markers, CD 86, IL ‐2 and ITGAX . These compensatory mechanisms resulted in markedly blunted levels of TNF ‐α, IL ‐12p40, MIP ‐1α, G‐ CSF and IL ‐6 in response to LPS challenge. Notably, exogenous supplementation of rh SP ‐D salvaged the WT mice from LPS ‐induced pro‐inflammatory immune response and impairment of sperm motility by upregulating the levels of TGF ‐β1 and IL ‐10. Conclusion The study highlights the involvement of SP ‐D in maintenance of testicular immune privilege and its indirect contribution to male fertility.