Pulmonary inflammation in XXXX exposed to mainstream cigarette smoke.

@entity32 @entity19 @entity1239 @entity2415 @entity7707
Male C57Bl/6 (C57) and ICR @entity19 were exposed by nose-only inhalation to mainstream cigarette smoke (MS) from 2R4F reference cigarettes, at concentrations of 75, 250, and 600 microg of total particulate matter (TPM) per liter, for up to 6 mo. Respiratory-tract tissue (nose, larynx, and lung), blood, and bronchoalveolar lavage fluid (BALF) samples were collected and analyzed at several time points. Blood samples were analyzed for biomarkers of exposure (COHb and @entity1239 ). BALF was analyzed for biomarkers of cell injury, @entity32 , oxidative stress, enzyme activity, and cytokines. Blood COHb and plasma @entity1239 concentrations increased in a dose-dependent manner, confirming smoke exposure. Mild @entity2415 was observed following 28 wk of exposure. Macrophage accumulation and inflammatory infiltrates were observed around the alveolar ducts and adjacent vasculature. There was an approximately 13% increase in mean linear intercept (Lm) only in ICR @entity19 exposed to 600 microg/L TPM. There were no significant changes in biomarkers of oxidative stress secondary to smoke exposures; however, @entity7707 significantly increased following the 13-wk post-inhalation period. BALF macrophage and neutrophil counts were rapidly and consistently elevated, while lymphocyte counts gradually increased over time. MS-induced inflammatory responses observed in this study are comparable to changes reported in chronic smokers, supporting the role of chronic @entity32 in the pathogenesis of @entity2415 . However, mild @entity2415 in minimal numbers of @entity19 suggests that MS exposure concentration and/or duration in the current study were not sufficient to induce a definitive @entity2415 phenotype.
