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Endotoxin and proinflammatory cytokines modulate Sertoli cell proliferation in vitro
Cecilia Petersen1, Berit Fröysa, Olle Söder
1Department of Women and Child Health, Paediatric Endocrinology Unit, Astrid Lindgren Children's Hospital, Karolinska Institutet and Hospital, Stockholm, Sweden. cecilia.petersen@kbh.ki.se
Journal of Reproductive Immunology
|March 19, 2004
Summary
Bacterial endotoxin (lipopolysaccharide; LPS) and tumor necrosis factor-alpha (TNF-alpha) directly stimulate Sertoli cell proliferation. Interleukin-6 (IL-6) and interferon-gamma (IFN-gamma) modulate FSH-induced Sertoli cell growth, impacting testicular development.
Area of Science:
- Reproductive Biology
- Endocrinology
- Immunology
Background:
- Sertoli cell number is crucial for adult germ cell production.
- Sertoli cell proliferation occurs during fetal and prepubertal development.
- Pathogenic influences during early life can impair testis development.
Purpose of the Study:
- To investigate the effects of bacterial endotoxin (lipopolysaccharide; LPS) and proinflammatory cytokines on early postnatal Sertoli cell development.
- To determine if LPS and cytokines influence Sertoli cell proliferation and survival.
Main Methods:
- Primary cultures of Sertoli cells from 8- to 9-day-old rats were used.
- Proliferation was assessed using (3)H-thymidine and BrdU incorporation assays.
- Cell viability was measured by supravital staining.
Main Results:
- LPS and TNF-alpha dose-dependently stimulated Sertoli cell proliferation in vitro.
- LPS significantly increased the number of viable Sertoli cells in culture.
- IL-6 and IFN-gamma did not directly affect Sertoli cell growth but modulated FSH-induced DNA synthesis (IL-6 increased, IFN-gamma inhibited).
Conclusions:
- Endotoxin and TNF-alpha are potent direct stimulators of Sertoli cell proliferation.
- IL-6 and IFN-gamma modulate the mitogenic action of FSH on immature Sertoli cells.
- These findings suggest a mechanism for testicular damage following infections and inflammation in early life, potentially disrupting adult germ cell production.