Exposure to cigarette smoke exacerbates polyhexamethylene guanidine-induced lung fibrosis in mice

Abstract

Cigarette smoke (CS) is the leading cause of chronic pulmonary diseases, including lung cancer, chronic obstructive pulmonary disease, and pulmonary fibrosis. In this study, we aimed to investigate the effects of repeated CS exposure on polyhexamethylene guanidine (PHMG)-induced pulmonary fibrosis in mice. A single intratracheal instillation of 0.6 mg/kg PHMG enhanced the immune response of mice by increasing the number of total and specific inflammatory cell types in the bronchoalveolar lavage fluid. It induced histopathological changes such as granulomatous inflammation/fibrosis and macrophage infiltration in the lungs. These responses were upregulated upon exposure to a combination of PHMG and CS. In contrast, a 4-hr/day exposure to 300 mg/m 3 CS alone for 2 weeks by nose-only inhalation resulted in minimal inflammation in the mouse lung. Furthermore, PHMG administration increased the expression of fibrogenic mediators, especially in the pulmonary tissues of the PHMG + CS group compared with that in the PHMG alone group. However, there was no upregulation in the expression of inflammatory cytokines following exposure to a combination of PHMG and CS. Our results demonstrate that repeated exposure to CS may promote the development of PHMG-induced pulmonary fibrosis.

Repeated intratracheal instillation of whole‐cigarette smoke condensate to assess lung damage in a rat model

“…Rats repeatedly exposed to cigarette smoke for 13 weeks displayed increased alveolar macrophages, pigmented and thickened alveolar walls, as well as hypertrophy/hyperplasia in the lungs 40 . In addition, it was confirmed that alveolar macrophage infiltration into the lungs of rats was mainly observed after repeated cigarette smoke exposure for 2 or 4 weeks 31,41 . The results of this study predict that repeated injection of WCSCs using ITI induced lung inflammation and damage similar to inhalation exposure.…”

“…40 In addition, it was confirmed that alveolar macrophage infiltration into the lungs of rats was mainly observed after repeated cigarette smoke exposure for 2 or 4 weeks. 31,41 The results of this study predict that repeated injection of WCSCs using ITI induced lung inflammation and damage similar to inhalation exposure. Our findings provide insight into the pulmonary inflammation response.…”

Environmental tobacco smoke exposure exaggerates bleomycin-induced collagen overexpression during pulmonary fibrogenesis

“…However, no clinical evidence showed how ETS exposure contributes to fibrogenesis development [ 12 , 32 ]. Recent animal studies have described that CS exacerbates the fibrotic progression induced by different causes such as bleomycin, lipopolysaccharides (LPS), polyhexamethylene guanidine, and influenza A virus (IAV) [ 3 , 6 , 7 , 33 , 34 ]. CS exposure followed by bleomycin administration showed significantly increased hydroxyproline and collagen deposition compared to bleomycin alone [ 3 , 6 ].…”

Evaluation of the Effects of e-Cigarette Aerosol Extracts and Tobacco Cigarette Smoke Extracts on RAW264.7 Cells

“…Macrophages, a crucial play in chronic diseases, can be adversely affected by CS, causing dysfunction . Repeated exposure to CS can also lead to macrophage infiltration and contribute to organ fibrosis development . Macrophages are vital for immunity and protecting the body from pathogens.…”