Eosinophilic airway inflammation induced by repeated exposure to cigarette smoke

Abstract

Acute exposure to cigarette smoke causes airway hyperresponsiveness (AHR) in guinea-pigs, which resolves within a few hours. Repeated exposure may have a different effect on the airways. To address this question, guinea-pigs were repeatedly exposed to cigarette smoke (six cigarettes for 1 h x day(-1)) for 14 consecutive days. Airway responsiveness to inhaled histamine and differential cell counts in bronchoalveolar lavage fluid (BALF) were evaluated 1 day after the last exposure. Significant neutrophilia in BALF was observed after 3 days of smoke exposure. Significant eosinophilia in BALF and AHR were observed after 14 days of smoke exposure, but not after 3 or 7 days of smoke exposure. These changes persisted until 3 days after the last exposure and resolved 7 days afterwards. Histologically, the recruited eosinophils were observed predominantly in the airways, but not in the alveoli. Treatment with E-6123, a specific platelet-activating factor receptor antagonist (1 mg x kg(-1) x day(-1) p.o. during smoke exposure) significantly inhibited the eosinophil influx and AHR. Repeated exposure to cigarette smoke may induce prolonged airway inflammation and airway hyperresponsiveness in guinea-pigs. Platelet-activating factor or platelet-activating factor-like lipids may play a key role in airway hyperresponsiveness, presumably by the induction of eosinophilic airway inflammation.

Leptin promotes the immune escape of lung cancer by inducing proinflammatory cytokines and resistance to apoptosis

“…Initiation of the immunoinflammatory lung response is induced by exposure to inhaled antigenic particles and is followed by an expression pattern of immunoinflammatory cytokines (25,26). Leptin is known to be upregulated upon sustained smoke exposure (24).…”

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

“…1998; Wright et al. 1999); however, we have described that at lower concentrations, they do not provide a toxic effect to macrophages, but rather affects their function.…”

Cytokine and chemokine expression in cigarette smoke-induced lung injury in guinea pigs

“…A commercially available nonfilter cigarette was used (Peace brand cigarettes; Japan Tobacco Inc., Tokyo, Japan) and, according to the manufacturer's specifications, each cigarette contained 2.4 mg of nicotine and 24 mg of tar. Referring to previous studies [8][9][10][11][12][13][14], the smoking conditions used in this study were determined based on the levels of BAL fluid (BALF) protein and total cell count. Each animal was placed into an individual chamber and exposed to diluted CS in a conscious and restrained state.…”

“…Among them, guinea pig CS models are considered to be adequate for further investigations of COPD because of the anatomical and pathophysiological similarities to human COPD [6]. It is generally accepted that shortterm CS exposure causes increased pulmonary permeability and accumulation of inflammatory cells [6,[8][9][10][11][12], and long-term exposure causes emphysematous airspace enlargement in the guinea pig models [12][13][14][15]. The guinea pig CS models have contributed to the current understanding of histological and physiological aspects of smoke-associated lung disease, but the underlying molecular mechanisms, including local production of cytokines and chemokines, are poorly understood because of the limited availability of research tools, such as specific antibodies for guinea pig proteins.…”