Increased expression of interleukin-1α and interleukin-1β is associated with experimental varicocele
Objective
To describe the effect of varicocele, in an experimental rat model, on the levels of IL-1α and IL-1β proteins in testis tissue.
Design
Comparative and controlled study.
Setting
Experimental research.
Animal(s)
Wistar male rats in experimental and control groups.
Intervention(s)
The control group underwent sham operation (n = 6). Experimental groups underwent partial ligation of the renal vein to induce experimental varicocele and were then killed at 9 (n = 6), 11 (n = 6), and 13 (n = 6) weeks after induction of varicocele.
Main Outcome Measure(s)
Histologic evaluation of the varicocele model was determined by periodic acid-Schiff staining of paraffin-embeded testicular tissues. Levels of cytokines were assessed by immunohistochemistry and Western blot analysis.
Result(s)
Varicocele caused testicular damage, especially in 11- and 13-week-old varicocele groups. In sham-operated rats, Golgi complexes of round spermatids expressed especially the α form of IL-1. By the progression of varicocele, the IL-1α expression increased temporally in Sertoli cells, spermatogonia, primary spermatocytes, spermatids, and Leydig cells. The expression of IL-1β was seen in Leydig cells in sham-operated rats. The IL-1β expression was also increased upon progression of varicocele in Leydig cells, Sertoli cells, and spermatogonia.
Conclusion(s)
We suggest that IL-1α and IL-1β are the regulators of testicular function. Certain pathologic conditions, e.g., varicocele, cause an increase in the expressions of such proinflammatory cytokines. The increased expression of IL-1α and IL-1β in varicocele shifts the balance in favor of inflammatory and immune responses and causes detrimental effects in testis tissue, which may cause male infertility.
Key Words: IL-1α , IL-1β , experimental varicocele , rat , testis
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This study was supported by Akdeniz University Research Foundation Antalya, Turkey, project number 2002.02.0122.003.
PII: S0015-0282(05)04201-9
doi:10.1016/j.fertnstert.2005.10.025
© 2006 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.

