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SUSCEPTIBILITY TO POLLUTANT-INDUCED AIRWAY INFLAMMATION IS NEUROGENICALLY MEDIATED.
Citation:
Roy, J., J D. Carter, M. Oortigisen, AND B Veronesi. SUSCEPTIBILITY TO POLLUTANT-INDUCED AIRWAY INFLAMMATION IS NEUROGENICALLY MEDIATED. Presented at 2000 Summer Neuropeptide Conference, Montreal, Canada, July 2000.
Description:
Neurogenic inflammation in the airways involves the activation of sensory irritant receptors (capsaicin, VR1) by noxious stimuli and the subsequent release of neuropeptides (e.g., SP, CGRP, NKA) from these fibers. Once released, these peptides initiate and sustain symptoms of inflammation (e.g., vasodilation, vasoconstriction, mucous secretion etc). Particulate matter (PM) is a major air pollutant that causes pulmonary inflammation in humans and experimental models. We have previously shown that the BALB/c mouse strain is responsive to PM-inflammation in contrast to the non-responsive C57/blk (B6) mouse strain. This differential sensitivity is retained in PM exposed cultures of somatosensory neurons from the dorsal root and trigeminal ganglia that innervate the airways in terms of inflammatory cytokine release. In the present study, we use RT-PCR, cobalt histochemistry and immunocytochemical techniques to show that the expression of capsaicin (VR1) and Substance P (NK-1) receptors and the release of inflammatory cytokines and neuropeptides are higher in sensory neurons from BALB/c mice relative to the B6 strain. These data suggest that the strain-specific inflammatory response to PM and other irritants (i.e. capsaicin, acid sensitive) seen in vivo and in vitro models of PM inflammation is subserved by sensory and neuropeptide receptors. (This abstract has been reviewed by NHEERL but does not necessarily reflect EPA policy).