Production of Superoxide and Nitric Oxide by Alveolar Macrophages in the Bleomycin-Induced Interstitial Pneumonia Mice Model

Yamazaki, C.; Hoshino, Jiro; Sekiguchi, Tomoko; Hori, Yusuke; Miyauchi, Satoshi; Mizuno, Syoji; Horie, Katsuyuki

doi:10.1254/jjp.78.69

Cited by 26 publications

(18 citation statements)

References 11 publications

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“…Stimulation of alveolar macrophages with LPS or bleomycin causes the production of large amounts of NO and superoxide, which together react to generate peroxynitrite (36,37). Furthermore, cigarette smoke is considered to activate alveolar macrophages to release inflammatory mediators, providing a cellular mechanism that links smoking with inflammation in COPD (chronic obstructive pulmonary disease) (38).…”

Section: Discussionmentioning

confidence: 99%

Oxidants in the Gas Phase of Cigarette Smoke Pass Through the Lung Alveolar Wall and Raise Systemic Oxidative Stress

et al. 2007

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Abstract. Cigarette smoking-induced oxidative stress plays a key role in the pathogenesis of atherosclerosis in smokers. Aqueous cigarette smoke extract (CSE) contains stable oxidants, peroxynitrite-like reactants, which have the ability to oxidize and nitrate low-density lipoprotein (LDL). We examined whether oxidants in CSE can penetrate into the blood through the lung alveolar wall and cause oxidative vascular injury. The oxidants in CSE and sodium peroxynitrite could easily pass through the reconstituted basement membrane. When CSE or sodium peroxynitrite solution was infused into the alveolar air space of an isolated rat lung mounted in tyrosine solution, CSE gradually increased the 3-nitrotyrosine levels in the external tyrosine solution while sodium peroxynitrite caused a rapid increase. CSE did not activate the rat alveolar macrophages. When rats were acutely exposed to the gas phase of cigarette smoke from which tar and nicotine had been removed, both serum levels of 3-nitrotyrosine and 8-hydroxy-2'-deoxyguanine, oxidative stress markers, rapidly increased. Our results demonstrate that relatively stable oxidants in CSE can pass through the pulmonary alveolar wall into the blood and induce systemic oxidative stress, which most likely facilitates oxidative modification of LDL and endothelial dysfunction, explaining early key events in the development of atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Oxidants in the Gas Phase of Cigarette Smoke Pass Through the Lung Alveolar Wall and Raise Systemic Oxidative Stress

et al. 2007

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“…On the other hand, activated inflammatory cells induced by cell damage in the lung release reactive oxygen and nitrogen species are also involved in the oxidant damage of the lung induced by BLM. 29) BLM cytotoxicity is prevented by superoxide dismutase in vitro, 30) and a number of antioxidants protect rodents from pulmonary injury and fibrosis. [8][9][10] Using this pulmonary fibrosis model, Feitai significantly decreased BLM-enhanced levels of LPO, suggesting that some antioxidants present in the formula may be involved in the protective mechanism against pulmonary fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Feitai Attenuates Bleomycin-Induced Pulmonary Fibrosis in Rats

Gong

Wang

et al. 2004

Biological & Pharmaceutical Bulletin

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Pulmonary fibrosis is a common consequence of numerous pulmonary diseases. The current therapeutic approaches for this condition are unsatisfactory. Feitai, a composite formula consisting of several herbs, is used in China as a folk remedy for treating patients with pulmonary tuberculosis. In this study, we extensively investigate the effects and mechanisms of Feitai on bleomycin (BLM)-induced pulmonary fibrosis in rats. One hundred and twenty male Sprague-Dawley rats were randomly divided into four groups, referred to as the saline-water, saline-Feitai, BLM-water, and BLM-Feitai groups. Following a single instillation of BLM (5 mg/kg) or saline, rats were orally administered Feitai at a dose of 3 g/kg body weight or sterilized distilled water once daily. Rats were killed at 7, 14, or 28 d post-BLM. Inflammatory cell count, protein concentration, and lactate dehydrogenase activity in bronchoalveolar lavage fluid were measured, and myeloperoxidase activity and lipid peroxide content in lung homogenates were analyzed. Treatment with Feitai inhibited lung fibrotic progression induced by BLM, as indicated by the decrease in lung hydroproline content and lung fibrosis score at 28 d post-BLM. This was accompanied by significant amelioration of BLM-induced body weight loss, lung edema, and inflammatory response during the development of lung injury in the acute phase. The results strongly indicate the beneficial effects of Feitai in protecting against BLM-induced pulmonary fibrosis. Furthermore, the inflammatory response and lipid peroxidation were inhibited by Feitai, suggesting that the effect of this formula on BLM-induced lung injury and fibrosis is associated with antiinflammatory and antioxidant properties.

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“…For instance, patients suffering from ARDS and premature infants requiring ventilation show increased incidence of protein modification (102,116,253) as assessed by nitrotyrosine formation (12, 133). Bleomycin-induced lung injury shows a similar effect (261,262,305). Inhaled NO treatment for ARDS is also associated with protein nitrotyrosine formation (159).…”

Section: Stressing Out the Neighborsmentioning

confidence: 94%

Sharing signals: connecting lung epithelial cells with gap junction channels

Koval

2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Gap junction channels enable the direct flow of signaling molecules and metabolites between cells. Alveolar epithelial cells show great variability in the expression of gap junction proteins (connexins) as a function of cell phenotype and cell state. Differential connexin expression and control by alveolar epithelial cells have the potential to enable these cells to regulate the extent of intercellular coupling in response to cell stress and to regulate surfactant secretion. However, defining the precise signals transmitted through gap junction channels and the cross talk between gap junctions and other signaling pathways has proven difficult. Insights from what is known about roles for gap junctions in other systems in the context of the connexin expression pattern by lung cells can be used to predict potential roles for gap junctional communication between alveolar epithelial cells.

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Production of Superoxide and Nitric Oxide by Alveolar Macrophages in the Bleomycin-Induced Interstitial Pneumonia Mice Model

Cited by 26 publications

References 11 publications

Oxidants in the Gas Phase of Cigarette Smoke Pass Through the Lung Alveolar Wall and Raise Systemic Oxidative Stress

Oxidants in the Gas Phase of Cigarette Smoke Pass Through the Lung Alveolar Wall and Raise Systemic Oxidative Stress

Feitai Attenuates Bleomycin-Induced Pulmonary Fibrosis in Rats

Sharing signals: connecting lung epithelial cells with gap junction channels

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