1. Effect of smoking cessation on chronic waterpipe smoke inhalation-induced airway hyperresponsiveness, inflammation, and oxidative stress
- Author
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Sumaya Beegam, Abderrahim Nemmar, Nur Elena Zaaba, Suhail Al-Salam, and Badreldin H. Ali
- Subjects
Male ,Pulmonary and Respiratory Medicine ,Physiology ,Smoke inhalation ,medicine.medical_treatment ,Airway hyperresponsiveness ,Water Pipe Smoking ,Inflammation ,030204 cardiovascular system & hematology ,medicine.disease_cause ,Pulmonary function testing ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Physiology (medical) ,Waterpipe Smoking ,Respiratory Hypersensitivity ,Animals ,Medicine ,Inhalation Exposure ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,business.industry ,NF-kappa B ,Cell Biology ,Smoke Inhalation Injury ,Catalase ,medicine.disease ,Glutathione ,Mice, Inbred C57BL ,Oxidative Stress ,030228 respiratory system ,Immunology ,Smoking cessation ,Female ,Smoking Cessation ,medicine.symptom ,business ,Oxidative stress ,DNA Damage - Abstract
Waterpipe smoking (WPS) prevalence is increasing globally. Clinical and laboratory investigations reported that WPS triggers impairment of pulmonary function, inflammation, and oxidative stress. However, little is known if smoking cessation (SC) would reverse the adverse pulmonary effects induced by WPS. Therefore, we evaluated the impact of WPS inhalation for 3 mo followed by 3 mo of SC (air exposure) compared with those exposed for either 3 or 6 mo to WPS or air (control) in C57BL/6 mice. To this end, various physiological, biochemical, and histological endpoints were evaluated in the lung tissue. Exposure to WPS caused focal areas of dilated alveolar spaces and foci of widening of interalveolar spaces with peribronchiolar moderate mixed inflammatory cells consisting of lymphocytes, macrophages, and neutrophil polymorphs. The latter effects were mitigated by SC. Likewise, SC reversed the increase of airway resistance and reduced the increase in the levels of myeloperoxidase, matrix metalloproteinase 9, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-α, interleukin (IL)-6, and IL-1β in lung tissue induced by WPS. In addition, SC attenuated the increase of oxidative stress markers including 8-isoprostane, glutathione, and catalase induced by WPS. Similarly, DNA damage, apoptosis, and the expression of NF-κB in the lung induced by WPS inhalation were alleviated by CS. In conclusion, our data demonstrated, for the first time, to our knowledge, that SC-mitigated WPS inhalation induced an increase in airway resistance, inflammation, oxidative stress, DNA injury, and apoptosis, illustrating the benefits of SC on lung physiology.
- Published
- 2021