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The present in vitro study in wall lizards Hemidactylus flaviviridis demonstrates the differential paracrine role of testicular macrophages in regulation of Leydig cell activities under normal physiological and inflammatory condition for the first time in reptiles. To accomplish the objective, the effect of condition media of testicular macrophages incubated in medium alone or with FSH/LPS was observed on Leydig cell steroidogenesis and proliferation. Non-activated testicular macrophage-conditioned medium (TMCM) increased the testosterone production from Leydig cells and the stimulation was more pronounced with FSH-preactivated TMCM, suggesting the trophic effect of FSH on secretion of steroidogenic factor from lizard testicular macrophages. Also, testicular macrophage-secreted paracrine factor had additive effect on FSH-induced testosterone production, since FSH-activated TMCM that contained both FSH as well as FSH-induced testicular macrophage-secreted paracrine factor, stimulated the Leydig cell steroidogenesis more potently than FSH alone. In contrast, LPS-activated TMCM inhibited the testosterone production suggesting the inhibitory role for testicular macrophages in control of Leydig cell steroidogenesis under inflammatory condition. Like steroidogenesis, the differential effects of TMCM were observed on Leydig cell proliferation depending on normal or inflammatory condition. Non-activated TMCM increased, while LPS-activated TMCM decreased the FSH-induced Leydig cell proliferation. It appears that lizard testicular macrophages under inflammatory condition secrete a different paracrine factor which instead of stimulating inhibits Leydig cell activities.

The present in vitro study, for the first time, demonstrates the endocrine as well as paracrine control of Leydig cell steroidogenesis and proliferation in the wall lizard Hemidactylus flaviviridis. Unlike mammals, Leydig cell activity in the wall lizard seems to be directly controlled by ovine follicle-stimulating hormone (FSH)-like molecule, since FSH increased the testosterone production and tritiated thymidine ([(3)H]TdR) incorporation by Leydig cells. In addition, Sertoli cell paracrine factor or factors play important roles in controlling Leydig cell activities as non-activated Sertoli cell-conditioned medium (SCCM) alone stimulated testosterone production by both non-activated and FSH-preactivated Leydig cells. As far as the proliferation was concerned, non-activated SCCM did not influence [(3)H]TdR uptake by non-activated or FSH-preactivated Leydig cells, while FSH-preactivated SCCM was able to stimulate proliferation of activated Leydig cells. It may be concluded that FSH, besides directly controlling, also regulates Leydig cell activities indirectly through stimulating the secretion of Sertoli cell paracrine factors. Moreover, steroidogenic factor is different from mitogenic factor because non-activated Leydig cells were responsive to steroidogenic factor but nonresponsive to mitogenic factor.