Antenatal exposure of maternal secondhand smoke (SHS) increases fetal lung expression of RAGE and induces RAGE-mediated pulmonary inflammation.

摘要: Background: Receptors for advanced glycation end-products (RAGE) are immunoglobulin-like pattern recognition receptors abundantly localized to lung epithelium. Our research demonstrated that primary tobacco smoke exposure increases RAGE expression and partly mediates pro-inflammatory signaling during exposure. However, the degree which influences developing lungs when gestating mice exposed secondhand (SHS) has not been determined date. Methods: Timed pregnant null wild type control were 4 consecutive days of SHS from embryonic day (E) 14.5 through E18.5 using a state art nose-only system (Scireq, Montreal, Canada). was assessed immunofluorescence, immunoblotting, quantitative RT-PCR. TUNEL immunostaining blotting caspase-3 performed evaluate effects on cell turnover. Matrix abnormalities discerned by quantifying collagen IV MMP-9, matrix metalloprotease capable degrading basement membranes. Lastly, TNF-α IL-1β levels in order determine inflammatory status lung. Results: Pulmonary elevated both dams fetuses within mothers SHS. Fetal weight, measure organismal health, decreased SHS-exposed pups, but unchanged mice. assessments suggested shift toward pulmonary apoptosis pups diminished as revealed increased MMP-9 expression. Furthermore, expressed less compared controls. Conclusions: augmentation maternal weakens deposition inflammation.