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

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Abstract
Summary: 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‐1α (IL‐1α) and β (IL‐1β), 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‐α (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‐1β 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.