Light cigarette smoke‐induced emphysema and NFkB activation in mouse lung

Abstract

Pulmonary emphysema is a common consequence of chronic cigarette smoke exposure. Although light cigarette (LC) exposure is supposed to be less hazardous, few experimental studies support this assumption. Our aim was to study lung injury by morphometrical and biochemical methods in mouse exposed to LC. C57BL/6 groups were subjected to smoke from 3, 6 or 12 LC for 60 days and compared to mice exposed to ambient air (EAA). Bronchoalveolar lavage (BAL), histology and stereology, lipid peroxidation (TBARS) and western blot were performed in mouse lungs. The cellular content of BAL was 95% alveolar macrophages in all groups except in mice exposed to 3 LC, where 23% neutrophils were observed. Emphysema was found in 12 LC parallel to increased volume density (Vv) of airspaces from 61.0±0.6 (EAA) to 80.9±1.0 (12 LC) and decreased Vv of elastic fibers from 17.8±0.9 (EAA) to 11.8±0.6 (12 LC). All exposed groups to LC showed low TBARS levels compared to EAA. Lung tissue from mouse exposed to 12 LC showed decreased TIMP-2 and increased MMP-12 detection, which suggests an imbalance in extracellular matrix (ECM). Increased TNF-α and NFκB detection were observed in exposed groups to LC when compared to EAA. The data suggest that LC is so dangerous to lungs as full-flavor cigarettes inducing ECM imbalance and emphysema. Supported by CAPES, FAPERJ and CNPq.