Cigarette Smoke Synergistically Enhances Respiratory Mucin Induction by Proinflammatory Stimuli

Baginski, Tomasz K.; Dabbagh, Karim; Satjawatcharaphong, Chiradath; Swinney, David C.

doi:10.1165/rcmb.2005-0259oc

Cited by 97 publications

(95 citation statements)

References 44 publications

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“…14) mice, 36,37) rats, 38) and dogs 39) by exposing the animals to sulfur dioxide (SO 2 ), 17) smoke from solid fuel, 19) cigarette smoke, 14,24,42) lipopolysaccharide, 39) proteases and their secretagogues, such as PAE, PPE, NE, proteinase 3, MMP, 44,48,49) and the factors used can enhance the effect of each other. 50,51) However, the rat model seems to be more economical and more feasible, and smoke and bacterial infections appear to be the most frequently used initiators. Although all of the factors used can induce COPD or emphysema-like pathophysiological pulmonary features, they are not similar to the disease occurring in patients with COPD.…”

Section: Discussionmentioning

confidence: 99%

A Rat Model for Stable Chronic Obstructive Pulmonary Disease Induced by Cigarette Smoke Inhalation and Repetitive Bacterial Infection

et al. 2012

Biological & Pharmaceutical Bulletin

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To develop a stable chronic obstructive pulmonary disease (COPD) model in rats. Sprague-Dawley rats were treated with cigarette-smoke inhalation (CSI) for 12 weeks, repetitive bacterial infection (RBI) for 8 weeks, or the combination of the two (CCR) for 12 weeks and followed up for the additional 20 weeks. Tidal volume (V T ), peak expiratory flow (PEF) and 50% V T expiratory flow (EF 50 ), histological changes in the lungs, and levels of the cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-8, and IL-10 in serum and bronchial alveolar lavage fluid (BALF) were examined at intervals during the 32 week study period. The right ventricular hypertrophy index (RVHI) was also determined at the same times. V T , PEF, and EF 50 were decreased in rats with COPD compared to the control. The expression of TNF-α, IL-8 and IL-10 increased in both serum and BALF with a similar trend. Bronchiole and arteriole wall thickness and the degree of bronchiole stenosis and alveolar size increased in COPD rats. RVHI was reduced gradually following the treatment. All of these changes were more pronounced in the CCR-treatment group than in the other groups. Our results have shown that CSI or RBI alone can induce COPD in rats, but that the combination of CSI with RBI induces a stable COPD that has more similarity to complications seen in patients with COPD. This combination may therefore provide a more appropriate model for study of human COPD.Key words pulmonary disease; chronic obstructive; animal model; pulmonary function; histological change; right ventricular hypertrophy index Chronic obstructive pulmonary disease (COPD) has been defined as a preventable and treatable pathologic condition characterized by partially reversible airflow limitation, 1) and is a major cause of morbidity and mortality throughout the world.2) Its prevalence among the Chinese population aged 40 or older is 8.2%.3) Development of COPD is slow and progressive in humans, with occasional exacerbations caused by an inflammatory response to triggering substances such as noxious gases, 1) bacteria 4-6) or viruses. [7][8][9][10][11] Four abnormalities are present in chronic, stable COPD: emphysema, small airway remodeling, pulmonary hypertension, and chronic bronchitis.Tobacco smoking and bacterial infection are the most common and important risk factors for COPD, 1,12,13) and they have each been used to establish animal COPD models. [14][15][16] Animal models have also used other noxious gases [17][18][19] and Pneumocystis carinii infection 20) in COPD induction. Short term induction protocols (days) 17,21) have resulted in a pulmonary inflammatory infiltrate, increased mucus production, and pulmonary edema. Long term induction protocols (weeks or months) 15,[17][18][19] have produced, in addition to the inflammatory infiltrate, emphysema and pulmonary remodeling characterized by fibrosis, and thickened bronchiole and arterial walls. Problems with animal models are that most of them are of short duration and the COPD produced does not correspond to the late...

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Section: Discussionmentioning

confidence: 99%

A Rat Model for Stable Chronic Obstructive Pulmonary Disease Induced by Cigarette Smoke Inhalation and Repetitive Bacterial Infection

et al. 2012

Biological & Pharmaceutical Bulletin

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“…Respiratory mucins protect the airway epithelium against exogenous insults. In chronic airway diseases, such as COPD, mucin hyperproduction contributes to airway obstruction, accelerated decline of lung function, morbidity and mortality [32]. Their hyperproduction is evoked by a variety of pro-inflammatory stimuli as a part of the inflammatory response in airways in COPD [31].…”

Section: Discussionmentioning

confidence: 99%

Moraxella catarrhalis induces ERK- and NF- B-dependent COX-2 and prostaglandin E2 in lung epithelium

N′Guessan

Temmesfeld-Wollbrück²,

Zahlten³

et al. 2007

European Respiratory Journal

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Moraxella catarrhalis is a major cause of infectious exacerbations of chronic obstructive lung disease. Cyclooxygenase (COX)-derived prostaglandins, such as prostaglandin E 2 (PGE 2 ), are considered to be important regulators of lung function. The present authors tested the hypothesis that M. catarrhalis induces COX-2-dependent PGE 2 production in pulmonary epithelial cells.In the present study, the authors demonstrate that M. catarrhalis specifically induces COX-2 expression and subsequent PGE 2 release in pulmonary epithelial cells. Furthermore, the prostanoid receptor subtypes EP2 and EP4 were also upregulated in these cells.The M. catarrhalis-specific ubiquitous cell surface protein A1 was important for the induction of COX-2 and PGE 2 . Moreover, M. catarrhalis-induced COX-2 and PGE 2 expression was dependent on extracellular signal-regulated kinase 1/2-driven activation of nuclear factor-kB, but not on the activation of p38 mitogen-activated protein kinase.In conclusion, the present data suggest that ubiquitous cell surface protein A1 of Moraxella catarrhalis, extracellular signal-regulated kinase 1/2 and nuclear factor-kB control cyclooxygenase-2 expression and subsequent prostaglandin E 2 release by lung epithelial cells. Moraxella catarrhalis-induced prostaglandin E 2 expression might counteract lung inflammation promoting colonisation of the respiratory tract in chronic obstructive pulmonary disease patients.

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“…In airway epithelial cells, MUC5AC secretion is considered an adaptive response to environmental stimuli such as respiratory viruses, 23 airway allergens, 24 and cigarette smoke. 25 We, and others, have demonstrated a requirement of autophagy for cell secretion of VWF (Von Willebrand factor) from endothelial cells, 26 lysozyme from intestinal Paneth cells, 27 and MUC2 from colonic goblet cells. 28,29 In each case, secretion requires the participation of ATG7 (autophagy-related 7), the ATG12-ATG5 conjugate and ATG16L1 (autophagy-related 16-like 1 [S. cerevisiae]) for autophagosome maturation and fusion.…”

Section: Introductionmentioning

confidence: 98%

IL13 activates autophagy to regulate secretion in airway epithelial cells

et al. 2016

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Cytokine modulation of autophagy is increasingly recognized in disease pathogenesis, and current concepts suggest that type 1 cytokines activate autophagy, whereas type 2 cytokines are inhibitory. However, this paradigm derives primarily from studies of immune cells and is poorly characterized in tissue cells, including sentinel epithelial cells that regulate the immune response. In particular, the type 2 cytokine IL13 (interleukin 13) drives the formation of airway goblet cells that secrete excess mucus as a characteristic feature of airway disease, but whether this process is influenced by autophagy was undefined. Here we use a mouse model of airway disease in which IL33 (interleukin 33) stimulation leads to IL13-dependent formation of airway goblet cells as tracked by levels of mucin MUC5AC (mucin 5AC, oligomeric mucus/gel forming), and we show that these cells manifest a block in mucus secretion in autophagy gene Atg16l1-deficient mice compared to wild-type control mice. Similarly, primary-culture human tracheal epithelial cells treated with IL13 to stimulate mucus formation also exhibit a block in MUC5AC secretion in cells depleted of autophagy gene ATG5 (autophagy-related 5) or ATG14 (autophagyrelated 14) compared to nondepleted control cells. Our findings indicate that autophagy is essential for airway mucus secretion in a type 2, IL13-dependent immune disease process and thereby provide a novel therapeutic strategy for attenuating airway obstruction in hypersecretory inflammatory diseases such as asthma, chronic obstructive pulmonary disease, and cystic fibrosis lung disease. Taken together, these observations suggest that the regulation of autophagy by Th2 cytokines is cell-context dependent.

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Cigarette Smoke Synergistically Enhances Respiratory Mucin Induction by Proinflammatory Stimuli

Cited by 97 publications

References 44 publications

A Rat Model for Stable Chronic Obstructive Pulmonary Disease Induced by Cigarette Smoke Inhalation and Repetitive Bacterial Infection

A Rat Model for Stable Chronic Obstructive Pulmonary Disease Induced by Cigarette Smoke Inhalation and Repetitive Bacterial Infection

Moraxella catarrhalis induces ERK- and NF- B-dependent COX-2 and prostaglandin E2 in lung epithelium

IL13 activates autophagy to regulate secretion in airway epithelial cells

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