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. 2012 Aug 28:3:348.
doi: 10.3389/fphys.2012.00348. eCollection 2012.

Pathogenic mechanism of second hand smoke induced inflammation and COPD

Rahel L Birru  1 , Y Peter Di
Affiliations

Pathogenic mechanism of second hand smoke induced inflammation and COPD

Rahel L Birru et al. Front Physiol. .

Abstract

Second hand smoke (SHS) introduces thousands of toxic chemicals into the lung, including carcinogens and oxidants, which cause direct airway epithelium tissue destruction. It can also illicit indirect damage through its effect on signaling pathways related to tissue cell repair and by the abnormal induction of inflammation into the lung. After repeated exposure to SHS, these symptoms can lead to the development of pulmonary inflammatory disorders, including chronic obstructive pulmonary disease (COPD). COPD is a severe pulmonary disease characterized by chronic inflammation and irreversible tissue destruction. There is no causal cure, as the mechanism behind the development and progression of the disease is still unknown. Recent discoveries implicate genetic predisposition associated with inflammatory response contributed to the development of COPD, linked to irregular innate and adaptive immunity, as well as a risk factor for cancer. The use of animal models for both cigarette smoke (CS) and SHS associated in vivo experiments has been crucial in elucidating the pathogenic mechanisms and genetic components involved in inflammation-related development of COPD.

Keywords: COPD; cancer; immunity; inflammation; second hand smoke.

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Figures

Figure 1
Figure 1
TS and LPS treated mice have enhanced inflammation and alveolar space enlargement. Mice were exposed to filtered air (A,B) or TS (C,D) generated by Kentucky Research Cigarettes for 6 months. Inflammation was further induced by intranasal LPS instillation (B,D), with saline as a control (A,C). Lung histology was analyzed by staining lung sections with hematoxylin and eosin. Results shown are representative images for each treatment at 10X magnification. TS-exposed mice displayed alveolar space enlargement (C) compared to filtered air exposure (A). LPS stimulated inflammatory cell influx (B) and enhanced the alveolar space enlargement induced by TS (D) relative to TS-only exposure (C).
See this image and copyright information in PMC

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