Cigarette Smoke-induced Airway Hyperresponsiveness Is Not Dependent on Elevated Immunoglobulin and Eosinophilic Inflammation in a Mouse Model of Allergic Airway Disease

Barrett, Edward G.; Wilder, Julie A.; March, Thomas H.; Espindola, Teresa; Bice, David E.

doi:10.1164/rccm.2106029

Cited by 59 publications

(58 citation statements)

References 59 publications

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“…Consistent with our data, greater inner airway wall thickness in infants who died of sudden infant death syndrome and who were born to mothers who smoked during pregnancy also suggests airway remodeling following in utero smoke exposure (10). The findings of Barrett et al (1), who report that exposure to sidestream smoke in a transgenic mouse model genetically predisposed to asthma was not associated with the development of allergic sensitization, further reinforce alternative mechanisms, such as pulmonary structural changes, as the possible mechanism for asthma in in utero smoke-exposed offspring. In contrast, some studies have reported higher IgE levels in the children of smoking parents (39).…”

Section: Discussionsupporting

confidence: 91%

PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring

Liu

Sakurai

O'Roark

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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Kenyon NJ, Torday JS, Rehan VK. PPAR␥ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring. Am J Physiol Lung Cell Mol Physiol 300: L710 -L717, 2011. First published February 25, 2011 doi:10.1152/ajplung.00337.2010.-Perinatal exposure to maternal smoke is associated with adverse pulmonary effects, including reduced lung function and increased incidence of asthma. However, the mechanisms underlying these effects are unknown, and there is no effective preventive and/or therapeutic intervention. Recently, we suggested that downregulation of homeostatic mesenchymal peroxisome proliferator-activated receptor-␥ (PPAR␥) signaling following in utero nicotine exposure might contribute to chronic lung diseases such as asthma. We used an in vivo rat model to determine the effect of perinatal nicotine exposure on 1) offspring pulmonary function, 2) mesenchymal markers of airway contractility in trachea and lung tissue, and 3) whether administration of a PPAR␥ agonist, rosiglitazone (RGZ), blocks the molecular and functional effects of perinatal nicotine exposure on offspring lung. Pregnant SpragueDawley rat dams received placebo, nicotine, or nicotine ϩ RGZ daily from embryonic day 6 until postnatal day 21, when respiratory system resistance, compliance, tracheal contractility, and the expression of markers of pulmonary contractility were determined. A significant increase in resistance and a decrease in compliance under basal conditions, with more pronounced changes following methacholine challenge, were observed with perinatal nicotine exposure compared with control. Tracheal constriction response and expression of mesenchymal markers of airway contractility were also significantly increased following perinatal nicotine exposure. Concomitant treatment with RGZ completely blocked the nicotine-induced alterations in pulmonary function, as well as the markers of airway contractility, at proximal and distal airway levels. These data suggest that perinatal smoke exposure-induced asthma can be effectively blocked by PPAR␥ agonists.pregnancy; peroxisome proliferator-activated receptor-␥; smoke THERE IS STRONG EPIDEMIOLOGICAL and experimental evidence that perinatal exposure to maternal smoking results in detrimental long-term effects on lung growth and function, including significant suppression of alveolarization and increased predisposition to asthma in the offspring (2, 4 -6, 9, 13-15, 17, 27, 30, 42, 44, 45, 49). Since the mechanisms underlying these adverse pulmonary effects remain incompletely understood, there are no effective preventive or therapeutic interventions. Recently, on the basis of in vitro and in vivo studies from our laboratory, we suggested that downregulation of homeostatic lung mesenchymal peroxisome proliferator-activated receptor-␥ (PPAR␥) signaling might be a key contributor to chronic lung diseases such as bronchopulmonary dysplasia and asthma (23,34,36,37,48). We previously showed that in vitro and in vivo nicotine exposures result in the downregulation of pulmo...

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Section: Discussionsupporting

confidence: 91%

PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring

Liu

Sakurai

O'Roark

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…As shown in Fig. 8B, treatment of mice with CS stimulated the methacholine-dependent increase in airway resistance (airway hyperresponsiveness to methacholine), as previously reported (5,27), and this response could be suppressed by the concomitant treatment of animals with PC-SOD (Fig. 8B).…”

Section: Effect Of Combination Application Of Pc-sod With Ipratropiumsupporting

confidence: 83%

Superiority of PC-SOD to other anti-COPD drugs for elastase-induced emphysema and alteration in lung mechanics and respiratory function in mice

Tanaka

Sato

Aoshiba

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Bronchodilators (such as ipratropium bromide), steroids (such as fluticasone propionate), and newly developed anti-inflammatory drugs (such as roflumilast) are used for patients with chronic obstructive pulmonary disease (COPD). We recently reported that lecithinized superoxide dismutase (PC-SOD) confers a protective effect in mouse models of COPD. We here examined the therapeutic effect of the combined administration of PC-SOD with ipratropium bromide on pulmonary emphysema and compared the effect of PC-SOD to other types of drugs. The severity of emphysema in mice was assessed by various criteria. Lung mechanics (elastance) and respiratory function (ratio of forced expiratory volume in the first 0.05 s to forced vital capacity) were assessed. Administration of PC-SOD by inhalation suppressed elastase-induced pulmonary emphysema, alteration of lung mechanics, and respiratory dysfunction. The concomitant intratracheal administration of ipratropium bromide did not alter the ameliorating effects of PC-SOD. Administration of ipratropium bromide, fluticasone propionate, or roflumilast alone did not suppress the elastase-induced increase in the pulmonary level of superoxide anion, pulmonary inflammatory response, pulmonary emphysema, alteration of lung mechanics, or respiratory dysfunction as effectively as did PC-SOD. PC-SOD, but not the other drugs, showed a therapeutic effect even when the drug was administered after the development of emphysema. PC-SOD also suppressed the cigarette smoke-induced pulmonary inflammatory response and increase in airway resistance. Based on these results, we consider that the inhalation of PC-SOD would be therapeutically beneficial for COPD.

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“…Therefore, it is possible that one of the factors that contribute to the exaggerated airway narrowing in patients with COPD may be an abnormality in the nature of airway smooth muscle. Experimental evidence has been reported that chronic exposure to cigarette smoke augments the in vivo responsiveness of airways to cholinergic agonists in rats (Xu et al, 1993), guinea pigs (Wu and Lee, 1999), and mice (Barrett et al, 2002). Although little is known concerning the effect of cigarette smoking in vivo on the contractility of airway smooth muscle ex vivo, we previously demonstrated that subacute exposure to cigarette smoke in vivo caused an augmented ACh-induced contraction with an upregulation of RhoA in bronchial smooth muscle ex vitro (Chiba et al, 2005).…”

Section: Introductionmentioning

confidence: 78%

Different effects of smoke from heavy and light cigarettes on the induction of bronchial smooth muscle hyperresponsiveness in rats

Sakai

Fujita

Watanabe

et al. 2011

J. Smooth Muscle Res.

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Cigarette smoking is one of the main risk factors in the development of chronic obstructive pulmonary disease (COPD). It has been suggested that an augmented agonistinduced, RhoA mediated Ca 2+ sensitization is responsible for the enhanced bronchial smooth muscle contraction induced by cigarette smoking. In the present study, to determine whether or not these phenomena are dependent on the degree of exposure to the components of cigarette smoke, we examined the effects of exposure to mainstream smoke derived from either light or heavy cigarettes on both the contractile responsiveness and the expression of RhoA in bronchial smooth muscle. Male Wistar rats were exposed to mainstream cigarette smoke for 2 hr/day for 2 weeks. Twenty-four hr after the last cigarette smoke exposure, we measured isometrical contractions of the bronchial smooth muscle. The concentration-response curve to ACh was significantly shifted upward after heavy cigarette smoke (HCS) exposure, whereas no significant difference was observed in the case of light cigarette smoke (LCS) exposure compared with control rats. No significant difference in K + responsiveness was observed between the groups. The expression of RhoA protein in bronchial preparations from rats repeatedly exposed to HCS, but not to LCS, was significantly increased as compared with that of the control animals. On the other hand, inhalation of nicotine had no effect on either the ACh-and high K + depolarizationinduced contractions or the expression of RhoA protein. The increased expression of RhoA seems to have an important role in the augmented contractile responses of the airways in rats, a characteristic feature of early COPD.

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Cigarette Smoke-induced Airway Hyperresponsiveness Is Not Dependent on Elevated Immunoglobulin and Eosinophilic Inflammation in a Mouse Model of Allergic Airway Disease

Cited by 59 publications

References 59 publications

PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring

PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring

Superiority of PC-SOD to other anti-COPD drugs for elastase-induced emphysema and alteration in lung mechanics and respiratory function in mice

Different effects of smoke from heavy and light cigarettes on the induction of bronchial smooth muscle hyperresponsiveness in rats

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