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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 and paracrine control of testicular macrophage activities in ectodermic vertebrates. Follicle-stimulating hormone (FSH) increased phagocytosis and superoxide production by macrophages. In regard to paracrine control, non-activated Leydig cell-conditioned medium (LCCM) decreased both the activities, whereas FSH-preactivated LCCM had differential effects: inhibitory on phagocytosis and stimulatory on superoxide production. However, FSH-activated LCCM, in addition to superoxide production, also enhanced phagocytosis. After heat inactivation, FSH-activated LCCM inhibited both the activities. Addition of FSH resulted in stimulation of phagocytosis, while partially restored the superoxide production. It can be speculated that androgen in heat-inactivated FSH-activated LCCM, in the presence of FSH, instead of inhibitory had stimulatory effect on phagocytosis, but remained inhibitory to superoxide production. Further, FSH-induced Leydig cell-secreted non-steroidal heat-labile factors appear to have stimulatory effect on superoxide production. This was corroborated by experiments with dihydrotestosterone in presence/absence of FSH.

The present study in the wall lizard, Hemidactylus flaviviridis, was aimed to understand the role of histamine (HA) in the regulation of Leydig cell and testicular macrophage activities, for the first time, in ectothermic vertebrates. Although HA did not affect the testosterone production from unstimulated Leydig cells, it had dual concentration-related effects, stimulatory at a low concentration of 10(-10) M while inhibitory at a high concentration of 10(-5) M, on FSH-induced testosterone production. This suggests that HA did not influence the basal Leydig cell steroidogenesis, but modulated the FSH-stimulated testosterone production in a biphasic manner depending upon its concentration. However, HA failed to affect the FSH-stimulated Leydig cell proliferation, indicating that HA modulated the testosterone production from Leydig cells without influencing their proliferation in wall lizards. HA, apart from Leydig cells, differentially regulated the testicular macrophage immune responses. It inhibited phagocytosis and superoxide production at high concentration (10(-5) M), while stimulated superoxide production and could not affect phagocytosis at low concentration (10(-10) M). Using selective H1 and H2 antagonists, pyrilamine and famotidine respectively, H1 receptor subtype was seen responsible for mediating the inhibitory effect of HA on Leydig cell steroidogenesis and testicular macrophage immune responses at high concentration, while H2 receptors were involved for the stimulation at low concentration.