In recent years, hydrogen sulfide (H₂ S) has been reported as a gaseous modulator acting in several tissues in health and disease. In animal models of systemic inflammation, the plasma H₂ S concentration increases in response to endotoxin (bacterial lipopolysaccharide, LPS). The most striking response in the acute phase reaction of systemic inflammation is fever, but we found no reports of the peripheral action of H₂ S on this thermoregulatory response. We aimed at investigating whether endogenous systemic H₂ S modulates LPS-induced fever. A temperature datalogger capsule was inserted in the abdominal cavity of male Wistar rats (220-270 g) to record body core temperature. These animals received an i.p. injection of a systemic H₂ S inhibitor (propargylglycine; 50 or 75 mg kg^-1 ), immediately followed by an i.p. injection of LPS (50 or 2500 μg kg^-1 ), and were exposed to different ambient temperatures (16, 22 or 27°C). At 22°C, but not at 27°C, propargylglycine at 75 mg kg^-1 significantly attenuated (P < 0.0001) the fever induced by LPS (50 μg kg^-1 ), indicating a modulatory (permissive) action of endogenous peripheral H₂ S on brown adipose tissue (BAT) thermogenesis. Evidence on the modulatory role of peripheral H₂ S in BAT thermogenesis was strengthened when we discarded (i) the possible influence of the gas on febrigenic signalling (when measuring plasma cytokines), and (ii) its interaction with the nitric oxide pathway, and mainly when (iii) we carried out physiological and pharmacological activations of BAT. Endogenous peripheral H₂ S modulates (permits) BAT activity not only in fever but also during maintenance of thermal homeostasis in cold environments.

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