Cigarette smoke-mediated inflammatory and oxidative responses are strain-dependent in mice

Yao, Hongwei; Edirisinghe, Indika; Saravanan, R.; Yang, Se‐Ran; Caito, Samuel; Adenuga, David; Rahman, Irfan

doi:10.1152/ajplung.00439.2007

Cited by 136 publications

(189 citation statements)

References 53 publications

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“…In contrast, the number of macrophages was not altered after 3-d CS exposure, whereas subchronic and chronic CS exposure induced a significant increase in macrophages influx in BAL fluid of C57BL/6J mice. These discrepancies are likely caused by differences in CS doses, and pattern/composition of smoke delivered by different CS generating systems (31,32).…”

Section: Discussionmentioning

confidence: 99%

“…All animal procedures described in this study were approved by the University Committee on Animal Research Committee of the University of Rochester. For studies involving 3-d CS exposure, research-grade cigarettes (3R4F; University of Kentucky, Lexington, KY) were used to generate smoke, and 8-wk-old male mice were exposed to mainstream CS using a BaumgartnerJaeger CSM2072i automatic CS generating machine (CH Technologies) as described previously (31). The smoke concentration was set at a value of approximately 300 mg TPM/m 3 (31,37).…”

Section: Methodsmentioning

confidence: 99%

“…For studies involving 3-d CS exposure, research-grade cigarettes (3R4F; University of Kentucky, Lexington, KY) were used to generate smoke, and 8-wk-old male mice were exposed to mainstream CS using a BaumgartnerJaeger CSM2072i automatic CS generating machine (CH Technologies) as described previously (31). The smoke concentration was set at a value of approximately 300 mg TPM/m 3 (31,37). Mice received two 1-h exposures (1 h apart) daily for 3 consecutive d, and were killed at 24 h after last exposure.…”

Section: Methodsmentioning

confidence: 99%

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Extracellular superoxide dismutase protects against pulmonary emphysema by attenuating oxidative fragmentation of ECM

Yao

Arunachalam

Hwang

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Extracellular superoxide dismutase (ECSOD or SOD3) is highly expressed in lungs and functions as a scavenger of O 2 • ─ . ECM fragmentation, which can be triggered by oxidative stress, participates in the pathogenesis of chronic obstructive pulmonary disease (COPD) through attracting inflammatory cells into the lungs. The level of SOD3 is significantly decreased in lungs of patients with COPD. However, the role of endogenous SOD3 in the development/progression of emphysema is unknown. We hypothesized that SOD3 protects against emphysema by attenuating oxidative fragmentation of ECM in mice. To test this hypothesis, SOD3-deficient, SOD3-transgenic, and WT C57BL/6J mice were exposed to cigarette smoke (CS) for 3 d (300 mg total particulate matter/m 3 ) to 6 mo (100 mg/m 3 total particulate matter) or by intratracheal elastase injection. Airspace enlargement, lung inflammation, lung mechanical properties, and exercise tolerance were determined at different time points during CS exposure or after elastase administration. CS exposure and elastase administration caused airspace enlargement as well as impaired lung function and exercise capacity in SOD3-null mice, which were improved in mice overexpressing SOD3 and by pharmacological SOD mimetic. These phenomena were associated with SOD3-mediated protection against oxidative fragmentation of ECM, such as heparin sulfate and elastin, thereby attenuating lung inflammatory response. In conclusion, SOD3 attenuates emphysema and reduces oxidative fragmentation of ECM in mouse lung. Thus, pharmacological augmentation of SOD3 in the lung may have a therapeutic potential in the intervention of COPD/emphysema.antioxidants | cigarette smoke | chronic obstructive pulmonary disease | oxidants | glutathione E xtracellular superoxide dismutase (ECSOD or SOD3) is one of the three SOD antioxidant enzyme isoforms, and is highly expressed in lungs and vessels (1, 2). It is located in the ECM, the junctions of airway epithelial cells, the surface of airway smooth muscle, and the lining of vessels of the lung. SOD3 functions as a superoxide anion scavenger, thereby attenuating oxidative stress, which may play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Acute loss of SOD3 in adult mice causes death, whereas low mortality rates are seen in SOD3-overexpressing animals exposed to hyperoxia, suggesting an essential role of SOD3 for survival (3,4). Accumulating evidence shows that SOD3 polymorphism is associated with a decline in lung function in rodents and humans, and susceptibility to COPD, which may be a result of alteration of its encoding protein structure, function, and level (5-14). However, it is unclear whether endogenous SOD3 participates in the development/ progression of the inflammatory response, leading to COPD/ emphysema.Cigarette smoke (CS) is the major etiological factor in the pathogenesis of COPD, which is characterized by chronic lung inflammation, parenchymal destruction (i.e., emphysema), and accelerated decline in lung function....

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Extracellular superoxide dismutase protects against pulmonary emphysema by attenuating oxidative fragmentation of ECM

Yao

Arunachalam

Hwang

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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175

166

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“…The term COPD includes at least two main lung diseases: chronic bronchitis and emphysema, both accompanied by airways remodelling and abnormal inflammatory responses of the lungs. Increased numbers of neutrophils, macrophages and inflammatory mediators are observed in the sputum and bronchoalveolar lavage fluid of COPD patients as well as in the lung of experimental animal models exposed to cigarette smoke (D'hulst et al, 2005;Yao et al, 2008;Braber et al, 2010). Cigarette smoke (either as gas phase or aqueous extract) acutely stimulates the release of interleukin-8 (IL-8) and tumour necrosis factor-a in macrophages (e.g.…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoke and α,β‐unsaturated aldehydes elicit VEGF release through the p38 MAPK pathway in human airway smooth muscle cells and lung fibroblasts

Volpi

Facchinetti

Moretto

et al. 2011

British J Pharmacology

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BACKGROUND AND PURPOSEVascular endothelial growth factor (VEGF) is an angiogenic factor known to be elevated in the sputum of asymptomatic smokers as well as smokers with bronchitis type of chronic obstructive pulmonary disease. The aim of this study was to investigate whether acute exposure to cigarette smoke extract altered VEGF production in lung parenchymal cells. EXPERIMENTAL APPROACHWe exposed human airway smooth muscle cells (ASMC), normal human lung fibroblasts (NHLF) and small airways epithelial cells (SAEC) to aqueous cigarette smoke extract (CSE) in order to investigate the effect of cigarette smoke on VEGF expression and release. KEY RESULTSVascular endothelial growth factor release was elevated by sub-toxic concentrations of CSE in both ASMC and NHLF, but not in SAEC. CSE-evoked VEGF release was mimicked by its component acrolein at concentrations (10-100 mM) found in CSE, and prevented by the antioxidant and a,b-unsaturated aldehyde scavenger, N-acetylcysteine (NAC). Both CSE and acrolein (30 mM) induced VEGF mRNA expression in ASMC cultures, suggesting an effect at transcriptional level. Crotonaldehyde and 4-hydroxy-2-nonenal, an endogenous a,b-unsaturated aldehyde, stimulated VEGF release, as did H2O2. CSE-evoked VEGF release was accompanied by rapid and lasting phosphorylation of p38 MAPK (mitogen-activated protein kinase), which was abolished by NAC and mimicked by acrolein. Both CSE-and acrolein-evoked VEGF release were blocked by selective inhibition of p38 MAPK signalling. CONCLUSIONS AND IMPLICATIONSa,b-Unsaturated aldehydes and possibly reactive oxygen species contained in cigarette smoke stimulate VEGF expression and release from pulmonary cells through p38 MAPK signalling.

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“…However, the molecular basis of susceptibility of mouse strains to effects of CS is not known. Previous studies have demonstrated that C57BL/6J mice responded to CS exposure with accelerated development of emphysema [1,2,3,4,5] while those of the strain 129S2/SvHsd, which produce low levels of tumor necrosis factoralpha (TNF-a), were resistant to lung inflammation and oxidant responses to CS exposure [4,5] showing no inflammatory response to smoke at 24 h [6].…”

Section: Introductionmentioning

confidence: 99%

Role of Recently Migrated Monocytes in Cigarette Smoke-Induced Lung Inflammation in Different Strain of Mice

Pérez-Rial

Terrón-Expósito

Girón-Martínez

et al. 2014

Chest

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This study investigates the role of proinflammatory monocytes recruited from blood circulation and recovered in bronchoalveolar lavage (BAL) fluid in mediating the lung damage in a model of acute cigarette smoke (CS)-induced lung inflammation in two strains of mice with different susceptibility to develop emphysema (susceptible -C57BL/6J and non susceptible -129S2/SvHsd). Exposure to whole-body CS for 3 consecutive research cigarettes in one single day induced acute inflammation in the lung of mice. Analysis of BAL fluid showed more influx of recently migrated monocytes at 72 h after CS-exposition in susceptible compared to non susceptible mice. It correlated with an increase in MMP-12 and TNF-a protein levels in the lung tissue, and with an increment of NF-kB translocation to the nucleus measured by electrophoretic mobility shift assay in C57BL/6J mice. To determine the functional role of these proinflammatory monocytes in mediating CS-induced airway inflammation, alveolar macrophages and blood monocytes were transiently removed by pretreatment with intratracheal and intravenous liposome-encapsulated CL 2 MDP, given 2 and 4 days prior to CS exposure and their repopulation was studied. Monocytes/macrophages were maximally depleted 48 h after last liposome application and subsequently recently migrated monocytes reappeared in BAL fluid of susceptible mice at 72 h after CS exposure. Recently migrated monocytes influx to the lung correlated with an increase in the MMP-12 protein level in the lung tissue, indicating that the increase in proinflammatory monocytes is associated with a major tissue damaging. Therefore our data confirm that the recruitment of proinflammatory recently migrated monocytes from the blood are responsible for the increase in MMP-12 and has an important role in the pathogenesis of lung disease induced by acute lung inflammation. These results could contribute to understanding the different susceptibility to CS of these strains of mice.

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Cigarette smoke-mediated inflammatory and oxidative responses are strain-dependent in mice

Cited by 136 publications

References 53 publications

Extracellular superoxide dismutase protects against pulmonary emphysema by attenuating oxidative fragmentation of ECM

Extracellular superoxide dismutase protects against pulmonary emphysema by attenuating oxidative fragmentation of ECM

Cigarette smoke and α,β‐unsaturated aldehydes elicit VEGF release through the p38 MAPK pathway in human airway smooth muscle cells and lung fibroblasts

Role of Recently Migrated Monocytes in Cigarette Smoke-Induced Lung Inflammation in Different Strain of Mice

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