Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments

Abstract

Cigarette smoking (CS) can impact the immune system and induce pulmonary disorders such as chronic obstructive pulmonary disease (COPD), which is currently the fourth leading cause of chronic morbidity and mortality worldwide. Accordingly, the most significant risk factor associated with COPD is exposure to cigarette smoke. The purpose of the present study is to provide an updated overview of the literature regarding the effect of CS on the immune system and lungs, the mechanism of CS-induced COPD and oxidative stress, as well as the available and potential treatment options for CS-induced COPD. An extensive literature search was conducted on the PubMed/Medline databases to review current COPD treatment research, available in the English language, dating from 1976 to 2014. Studies have investigated the mechanism by which CS elicits detrimental effects on the immune system and pulmonary function through the use of human and animal subjects. A strong relationship among continued tobacco use, oxidative stress, and exacerbation of COPD symptoms is frequently observed in COPD subjects. In addition, therapeutic approaches emphasizing smoking cessation have been developed, incorporating counseling and nicotine replacement therapy. However, the inability to reverse COPD progression establishes the need for improved preventative and therapeutic strategies, such as a combination of intensive smoking cessation treatment and pharmaceutical therapy, focusing on immune homeostasis and redox balance. CS initiates a complex interplay between oxidative stress and the immune response in COPD. Therefore, multiple approaches such as smoking cessation, counseling, and pharmaceutical therapies targeting inflammation and oxidative stress are recommended for COPD treatment.

Resolvin D1 Reduces Emphysema and Chronic Inflammation

“…Cigarette smoke contains high levels of free radicals and free radicalegenerating compounds that contribute to oxidative stress. 7 However, it is also clear that a second significant source of oxidative stress in chronic lung disease including COPD are inflammatory cells themselves. 5,8 Cigarette smoke and oxidative stress are both strong stimulators of cell death and are key factors in the tissue destruction seen in emphysema.…”

“…Activated macrophages and neutrophils can produce superoxide, nitric oxide, peroxynitrite, hydrogen peroxide, and hypochlorite. 5,7,8 This production generates the potential for a proinflammatory feed-forward loop that promotes continued chronic inflammation and tissue damage even after smoking cessation. 4 It is now widely acknowledged that the resolution of inflammation is a programed, self-limited process governed by a group of bioactive lipid mediators, coined specialized proresolving lipid mediators (SPMs).…”

Imaging Pulmonary Inflammation

“…COPD is a heterogeneous disease that is defined by progressive, irreversible airflow limitation. The lungs' inflammatory response to the inhalation of particles and gases, particularly from cigarette smoke, is thought to cause lung tissue injury and destruction, thus leading to the development of COPD (39,40). Evidence suggest that macrophages drive the development of COPD, leading to increased neutrophil recruitment in the airways (41,42).…”

Occupational Exposures and Chronic Obstructive Pulmonary Disease. Causality Established, Time to Focus on Effect and Phenotypes

“…Chronic obstructive pulmonary disease (COPD) is complex and is the result, among susceptible hosts, of the interaction of repeated environmental injurious exposures and abnormal host defense or reparative mechanisms (1,2). In addition to an intricate pathogenesis, a variable progression and disease expression (3) are responsible for difficulties in ascertaining causality at the individual level and hence in accurately determining to what extent the societal burden of disease is a result of one specific exposure, and designing appropriate preventive or mitigating interventions, to ameliorate the impact of the disease.…”

“…In 2007, 2010, and now again in 2015, the American Thoracic Society has recommended that the U.S. Environmental Protection Agency (EPA) adopt an 8-hour ozone national ambient air quality standard of 60 ppb to adequately protect public health (1,2). Although the recommended standard endorsed by the American Thoracic Society has not changed during this time, the scientific evidence supporting this recommendation has significantly strengthened.…”