Human chorionic gonadotrophin-induced testicular inflammation may be related to increased sensitivity to interleukin-1.

Treatment of adult male rats with human chorionic gonadotrophin (hCG) results in an inflammation-like response in the testicular microcirculation. Polymorphonuclear (PMN) leukocytes accumulate in venules and vascular permeability is increased. The mechanism behind this response was studied. Treatment with an interleukin-1 receptor antagonist partly prevented the hCG induced accumulation of PMN leukocytes 4 h after treatment. Human recombinant interleukin-1 alpha (IL-1 alpha) and beta (IL-1 beta), serotonin, and histamine were injected intratesticularly on one side and saline injected on the contralateral side in both intact and hCG-pretreated adult rats. A low dose of IL-alpha (a dose that did not increase vascular permeability in unstimulated testes) increased vascular permeability in the testes of animals treated with hCG 4, 6 or 8 h earlier, but it was without effect in testes from rats treated with hCG 0,1, 2, 16 or 32 h prior to IL-1 injection. The sensitivity to the pro-inflammatory effect of locally injected IL-1 beta was also increased by hCG treatment. There was no increase in vascular permeability after local injection of a large dose of histamine or serotonin in either saline- or in hCG-pretreated animals. Hypothetically, the hCG-induced inflammation-like increase in testicular vascular permeability could be related to increased sensitivity to constitutively produced mediators such as IL-1.