Sensory Neural Responses to Ozone Exposure during Early Postnatal Development in Rat Airways

摘要: Airway infections or irritant exposures during early postnatal periods may contribute to the onset of childhood asthma. The purpose this study was examine critical airway development which ozone (O(3)) exposure leads heightened neural responses. Rats were exposed O(3) (2 ppm) filtered air for 1 hour on specific days (PDs) between PD1 and PD29, killed 24 hours after exposure. In a second experiment, rats PD2-PD6, inside proposed period development, PD19-PD23, outside period. Both groups re-exposed PD28, later. Airways removed, fixed, prepared substance P (SP) immunocytochemistry. SP nerve fiber density (NFD) in control extrapulmonary (EXP) epithelium/lamina propria (EPLP) increased threefold, from 1% 3.3% PD1-PD3 through PD13-PD15, maintained PD29. Upon exposure, SP-NFD EXP-smooth muscle (SM) intrapulmonary (INT)-SM at least twofold PD13-PD15 comparison No change observed PD21-PD22 PD28-PD29. studies, INT-SM EXP-SM PD2-PD6 group PD28 significantly higher than that PD19-PD23 PD28. These findings suggest O(3)-mediated changes sensory innervation SM are more responsive earlier development. Enhanced responsiveness nerves be contributing mechanism susceptibility environmental human infants children.