| First Author | Graham RM | Year | 2001 |
| Journal | Am J Respir Crit Care Med | Volume | 164 |
| Issue | 2 | Pages | 307-13 |
| PubMed ID | 11463606 | Mgi Jnum | J:133168 |
| Mgi Id | MGI:3777885 | Doi | 10.1164/ajrccm.164.2.2007115 |
| Citation | Graham RM, et al. (2001) Sensory nerves promote ozone-induced lung inflammation in mice. Am J Respir Crit Care Med 164(2):307-13 |
| abstractText | 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. |
