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Role of substance P in hydrogen sulfide-induced pulmonary inflammation in mice

Department of Pharmacology, National University of Singapore, Singapore

Submitted 13 February 2006 ; accepted in final form 19 June 2006

We have shown earlier that H₂S acts as a mediator of inflammation. In this study, we have investigated the involvement of substance P and neurogenic inflammation in H₂S-induced lung inflammation. Intraperitoneal administration of NaHS (1–10 mg/kg), an H₂S donor, to mice caused a significant increase in circulating levels of substance P in a dose-dependent manner. H₂S alone could also cause lung inflammation, as evidenced by a significant increase in lung myeloperoxidase activity and histological evidence of lung injury. The maximum effect of H₂S on substance P levels and on lung inflammation was observed 1 h after NaHS administration. At this time, a significant increase in lung levels of TNF- and IL-1 was also observed. In substance P-deficient mice, the preprotachykinin-A knockout mice, H₂S did not cause any lung inflammation. Furthermore, pretreatment of mice with CP-96345 (2.5 mg/kg ip), an antagonist of the neurokinin-1 (NK₁) receptor, protected mice against lung inflammation caused by H₂S. However, treatment with antagonists of NK₂, NK₃, and CGRP receptors did not have any effect on H₂S-induced lung inflammation. Depleting neuropeptide from sensory neurons by capsaicin (50 mg/kg sc) significantly reduced the lung inflammation caused by H₂S. In addition, pretreatment of mice with capsazepine (15 mg/kg sc), an antagonist of the transient receptor potential vanilloid-1, protected mice against H₂S-induced lung inflammation. These results demonstrate a key role of substance P and neurogenic inflammation in H₂S-induced lung injury in mice.

neurogenic inflammation; lung injury; preprotachykinin-A; transient receptor potential vanilloid

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