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Am J Physiol Lung Cell Mol Physiol 291: L896-L904, 2006. First published June 23, 2006; doi:10.1152/ajplung.00053.2006
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Role of substance P in hydrogen sulfide-induced pulmonary inflammation in mice

Madhav Bhatia, Liang Zhi, Huili Zhang, Siaw-Wei Ng, and Philip K. Moore

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-{alpha} and IL-1beta 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


Address for reprint requests and other correspondence: M. Bhatia, Dept. of Pharmacology, National Univ. of Singapore, Yong Loo Lin School of Medicine, Bldg. MD2, 18 Medical Dr., Singapore 117597 (e-mail: mbhatia{at}nus.edu.sg)




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