Cigarette Smoke, Inflammation, and Lung Injury: A Mechanistic Perspective

Abstract

Inflammation is a common feature in the pathogenesis of cigarette smoke-associated diseases. The recruitment of inflammatory cells into the lung following cigarette smoke exposure presents a risk of tissue damage through the release of toxic mediators, including proteolytic enzymes and reactive oxygen species. This review represents a toxicological approach to investigation of cigarette smoke-induced lung injury, with a focus on laboratory studies and an emphasis on inflammatory mechanisms. The studies discussed in this review analyze the role of inflammation and inflammatory mediators in the development of injury. In cases where information relating to cigarette smoke is limited, examples are taken from other models of lung injury applicable to cigarette smoke. The primary aim of the review is to summarize published work so as to permit (1) an evaluation of chronic lung injury and inflammatory responses in animal models, (2) a discussion of inflammatory mediators in the development of chronic injury, and (3) identification of immunological mechanisms of injury. These studies discuss the currently understood roles of cytokines, cell adhesion molecules, and oxidative stress in inflammatory reactions and lung injury. A role for lipocortin 1 (annexin 1), a naturally occurring defense factor against inflammation, is discussed because of the possibility that impaired synthesis and degradation of lipocortin 1 will influence immune responses in animals exposed to cigarette smoke either by augmenting T helper cell Th1 response or by shifting Th1 to Th2 response. While Th1 augmentation will increase the risk for development of emphysema, Th1 to Th2 shift will favor development of asthma.

Claudin-3 and Clara Cell 10 kDa Protein as Early Signals of Cigarette Smoke–Induced Epithelial Injury along Alveolar Ducts

“…Neutrophil accumulation in pulmonary parenchyma is one of the hallmarks of both COPD and cigarette smoke models of COPD (Bhalla et al 2009;Di Stefano et al 1998; Stanescu FIGURE 14.-Severity and frequency of alveolar duct lining cell injury by cigarette smoke. The frequency and severity of epithelial changes along alveolar ducts decreased significantly from day 5 after exposure.…”

Reference Value Profile for Healthy Individuals From the Aljouf region of Saudi Arabia

“…Total cholesterol and triglyceride were also investigated, because IDA is associated by alteration in these parameters, which responds to iron treatment [12] and other anemia as well [13,14]. Participants who were diabetic, smoking, pregnant or lactating were also excluded from the study, as they cause alteration in hematological parameters [15][16][17][18]. Table 1 shows the normal values of each parameter in adults (male and female) and demonstrated significant variations in males versus females as reported in the previous studies [19,20].…”

Mechanisms of suppression of alveolar epithelial cell GM-CSF expression in the setting of hyperoxic stress

“…Inflammation driven by neutrophils or mononuclear phagocytes, ischemia-reperfusion injury, toxic inhalations (ozone, cigarette smoke, sulfur dioxide), and high concentrations of oxygen all induce significant oxidative stress in the lung (7,9,21). Although oxygen therapy is an essential component of supportive care for many patients, breathing high concentrations of oxygen may lead to lung injury, impaired barrier function of the alveolar wall, and death (16).…”