Evaluation of the pulmonary effects of short-term nose-only cigarette smoke exposure in mice

Abstract

Much is known about the chronic effects of cigarette smoke (CS) on lung function and inflammation and development of chronic obstructive pulmonary disease. However, the underlying pathophysiological mechanisms related to the short-term exposure to CS are not fully understood. Here, we assessed the effect of CS generated by nine consecutive cigarettes per day for four days in a nose-only exposure system on airway resistance measured using forced oscillation technique, lung inflammation and oxidative stress in BALB/c mice. Control mice were exposed to air. Mice exposed to CS showed a significant increase of neutrophils and lymphocytes numbers in bronchoalveolar lavage (BAL). The total protein and endothelin levels in BAL fluid were significantly augmented suggesting an increase of alveolar-capillary barrier permeability. Similarly, airway resistance was significantly increased in the CS group compared with controls. Furthermore, reactive oxygen species and lipid peroxidation levels in lung tissue were significantly increased. The antioxidant activities of reduced glutathione, glutathione S transferase and superoxide dismutase were all significantly increased following CS exposure, indicating that CS could trigger adaptive responses that counterbalance the potentially damaging activity of oxygen radicals induced by CS exposure. In conclusion, our data indicate that short-term nose-only exposure to CS causes lung inflammation and increase of airway resistance mediated at least partly through the oxidative stress.

Cardiovascular effects of nose-only water-pipe smoking exposure in mice

“…After 1 wk of acclimatization, animals were randomly divided into air (control) and WPS-exposed groups. Mice were placed in soft restraints and connected to the exposure tower (29,30,33). They were exposed to WPS or air through their noses using a nose-only exposure system (InExpose System, Scireq).…”

“…Homogenates were centrifuged for 10 min at 3,000 g to remove cellular debris, and supernatants were used for further analysis. Protein content was measured by Bradford's method as previously described (29,30).…”

“…ROS were measured in whole cardiac tissue homogenates, which were obtained as described above, using 2=,7=-dichlorofluorescein diacetate (Molecular Probes, Eugene, OR) as a fluorescent probe as previously described (29,30). The results were normalized as ROS produced per milligram of protein.…”

“…The results were normalized as ROS produced per milligram of protein. NADPH-dependent membrane lipid peroxidation (LPO) was measured as thiobarbituric acid-reactive substances using malonedialdehyde as the standard (Sigma-Aldrich, St. Louis, MO) (29,30).…”

Genetic variation associates with susceptibility for cigarette smoke-induced neutrophilia in mice

“…CS-induced airway inflammation can already occur after short-term exposure in individuals susceptible for the development of COPD (39,51). To date, little is known about the genetics of CS-induced neutrophilic airway inflammation, in contrast to the genetics of COPD or asthma for which many susceptibility genes have been identified (8,38).…”