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Am. J. Respir. Crit. Care Med., Volume 164, Number 2, July 2001, 307-313

Sensory Nerves Promote Ozone-induced Lung Inflammation in Mice

REGINA M. GRAHAM, MITCHELL FRIEDMAN, and GARY W. HOYLE

Section of Pulmonary Diseases, Critical Care and Environmental Medicine, Department of Medicine, and Tulane/Xavier Center for Bioenvironmental Research, Tulane University Health Sciences Center, New Orleans, Louisiana; and Graduate Program in Molecular and Cellular Biology, Tulane University, New Orleans, Louisiana

Genetically manipulated mice exhibiting altered innervation of the airways were used to examine the role of sensory nerves in ozone-induced lung inflammation. Transgenic mice expressing nerve growth factor (NGF) from the lung-specific Clara cell secretory protein (CCSP) promoter exhibit hyperinnervation of the airways by sympathetic and tachykinin-containing sensory nerve fibers. Mice carrying a mutation in the low-affinity NGF receptor (NGFR) gene possess deficits in sensory innervation. CCSP-NGF transgenic mice exhibited a twofold increase in the number of lung lavage neutrophil level whereas NGFR knockout mice exhibited a nearly 50% decrease in neutrophilic inflammation compared with wild-type mice 18 h after ozone inhalation. Treatment with neurokinin receptor antagonists reduced the level of neutrophilic inflammation in both wild-type and CCSP-NGF mice. Examination of lavage fluid cytokine concentrations revealed that 4 h after ozone exposure CCSP-NGF mice produced significantly higher amounts of the chemokine KC than wild-type mice exposed to ozone. The results of this study indicate that sensory nerves are important mediators of ozone-induced inflammation in mice.




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