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      Nrf2 Regulates the Risk of a Diesel Exhaust Inhalation-Induced Immune Response during Bleomycin Lung Injury and Fibrosis in Mice

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          Abstract

          The present study investigated the effects of diesel exhaust (DE) on an experimental model of bleomycin (BLM)-induced lung injury and fibrosis in mice. BLM was intravenously administered to both Nrf2 +/+ and Nrf2 −/− C57BL/6J mice on day 0. The mice were exposed to DE for 56 days from 28 days before the BLM injection to 28 days after the BLM injection. Inhalation of DE induced significant inhibition of airway clearance function and the proinflammatory cytokine secretion in macrophages, an increase in neutrophils, and severe lung inflammatory injury, which were greater in Nrf2 −/− mice than in Nrf2 +/+ mice. In contrast, inhalation of DE was observed to induce a greater increase of hydroxyproline content in the lung tissues and significantly higher pulmonary antioxidant enzyme mRNA expression in the Nrf2 +/+ mice than in Nrf2 −/− mice. DE is an important risk factor, and Nrf2 regulates the risk of a DE inhalation induced immune response during BLM lung injury and fibrosis in mice.

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          Excessive Neutrophils and Neutrophil Extracellular Traps Contribute to Acute Lung Injury of Influenza Pneumonitis

          Teluguakula Narasaraju, Edwin Yang, Ramar Samy … (2011)
          Complications of acute respiratory distress syndrome (ARDS) are common among critically ill patients infected with highly pathogenic influenza viruses. Macrophages and neutrophils constitute the majority of cells recruited into infected lungs, and are associated with immunopathology in influenza pneumonia. We examined pathological manifestations in models of macrophage- or neutrophil-depleted mice challenged with sublethal doses of influenza A virus H1N1 strain PR8. Infected mice depleted of macrophages displayed excessive neutrophilic infiltration, alveolar damage, and increased viral load, later progressing into ARDS-like pathological signs with diffuse alveolar damage, pulmonary edema, hemorrhage, and hypoxemia. In contrast, neutrophil-depleted animals showed mild pathology in lungs. The brochoalveolar lavage fluid of infected macrophage-depleted mice exhibited elevated protein content, T1-α, thrombomodulin, matrix metalloproteinase-9, and myeloperoxidase activities indicating augmented alveolar-capillary damage, compared to neutrophil-depleted animals. We provide evidence for the formation of neutrophil extracellular traps (NETs), entangled with alveoli in areas of tissue injury, suggesting their potential link with lung damage. When co-incubated with infected alveolar epithelial cells in vitro, neutrophils from infected lungs strongly induced NETs generation, and augmented endothelial damage. NETs induction was abrogated by anti-myeloperoxidase antibody and an inhibitor of superoxide dismutase, thus implying that NETs generation is induced by redox enzymes in influenza pneumonia. These findings support the pathogenic effects of excessive neutrophils in acute lung injury of influenza pneumonia by instigating alveolar-capillary damage.
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            Association between mortality and indicators of traffic-related air pollution in the Netherlands: a cohort study.

            Gerard Hoek, Bert Brunekreef, Sandra Goldbohm … (2002)
            Long-term exposure to particulate matter air pollution has been associated with increased cardiopulmonary mortality in the USA. We aimed to assess the relation between traffic-related air pollution and mortality in participants of the Netherlands Cohort study on Diet and Cancer (NLCS), an ongoing study. We investigated a random sample of 5000 people from the full cohort of the NLCS study (age 55-69 years) from 1986 to 1994. Long-term exposure to traffic-related air pollutants (black smoke and nitrogen dioxide) was estimated for the 1986 home address. Exposure was characterised with the measured regional and urban background concentration and an indicator variable for living near major roads. The association between exposure to air pollution and (cause specific) mortality was assessed with Cox's proportional hazards models, with adjustment for potential confounders. 489 (11%) of 4492 people with data died during the follow-up period. Cardiopulmonary mortality was associated with living near a major road (relative risk 1.95, 95% CI 1.09-3.52) and, less consistently, with the estimated ambient background concentration (1.34, 0.68-2.64). The relative risk for living near a major road was 1.41 (0.94-2.12) for total deaths. Non-cardiopulmonary, non-lung cancer deaths were unrelated to air pollution (1.03, 0.54-1.96 for living near a major road). Long-term exposure to traffic-related air pollution may shorten life expectancy.
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              Idiopathic pulmonary fibrosis.

              T J Gross, G W Hunninghake (2001)
              Idiopathic pulmonary fibrosis is a rapidly progressive illness of unknown cause characterized by sequential acute lung injury with subsequent scarring and end-stage lung disease. Treatment at present remains largely supportive, with evidence that patients' satisfaction and survival may be improved by referral to centers specializing in the evaluation of interstitial lung diseases. Although no drug therapy has clearly been demonstrated to benefit patients with idiopathic pulmonary fibrosis, a number of novel investigational agents hold promise for future study. Given the poor prognosis associated with idiopathic pulmonary fibrosis, patients should be referred to regional centers of expertise for enrollment in therapeutic clinical trials or for lung transplantation.
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                Author and article information

                Contributors
                Paul R. Reynolds: Role: Academic Editor
                Benjamin T. Bikman: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 17 March 2017
                Publication date Collection: March 2017
                Volume: 18
                Issue: 3
                Electronic Location Identifier: 649
                Affiliations
                [1 ]Department of Hygiene and Public Health, Nippon Medical School, Tokyo 113-0031, Japan; takako-s@ 123456nms.ac.jp (T.S.); yuki-hir@ 123456nms.ac.jp (Y.H.); hrfmi@ 123456nms.ac.jp (H.I.); kawada@ 123456nms.ac.jp (T.K.)
                [2 ]The Center for Environmental Health Science for the Next Generation, Research Institute for Science and Technology, Tokyo University of Science, Noda 278-8510, Japan; shinkai49@ 123456gmail.com (Y.S.); takedak@ 123456rs.noda.tus.ac.jp (K.T.)
                [3 ]Department of Pulmonary Medicine/Infection and Oncology, Nippon Medical School, Tokyo 113-8602, Japan; azuma_arata@ 123456yahoo.co.jp
                [4 ]Department of Biochemistry, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan; masiyamamoto@ 123456med.tohoku.ac.jp
                Author notes
                [* ]Correspondence: li-yingji@ 123456nms.ac.jp ; Tel.: +81-3-3822-2131; Fax: +81-3-5685-3065
                Article
                Publisher ID: ijms-18-00649
                DOI: 10.3390/ijms18030649
                PMC ID: 5372661
                PubMed ID: 28304344
                SO-VID: d531a0a8-afbd-4270-a374-d017ac2c323c
                Copyright © © 2017 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 28 January 2017
                Date accepted : 09 March 2017
                Categories
                Subject: Article

                ScienceOpen disciplines: Molecular biology
                Keywords: diesel exhaust,bleomycin,lung injury and fibrosis,nrf2,oxidative stress/antioxidative stress
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: diesel exhaust, bleomycin, lung injury and fibrosis, nrf2, oxidative stress/antioxidative stress

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