Immune‐pineal axis protects rat lungs exposed to polluted air
Environmental pollution in the form of particulate matter
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| Veröffentlicht in: | Journal of pineal research 2020-04, Vol.68 (3), p.e12636-n/a |
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| container_title | Journal of pineal research |
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| creator | Carvalho‐Sousa, Claudia Emanuele Pereira, Eliana P. Kinker, Gabriela S. Veras, Mariana Ferreira, Zulma S. Barbosa‐Nunes, Fernanda P. Martins, Joilson O. Saldiva, Paulo H.N. Reiter, Russel J. Fernandes, Pedro A. da Silveira Cruz‐Machado, Sanseray Markus, Regina P. |
| description | Environmental pollution in the form of particulate matter |
| doi_str_mv | 10.1111/jpi.12636 |
| format | Article |
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Our goal was to show that PM2.5 eliciting a proinflammatory response activates the immune‐pineal axis, reducing the pineal synthesis and increasing the extrapineal synthesis of melatonin. Herein, we report that the exposure of rats to polluted air for 6 hours reduced nocturnal plasma melatonin levels and increased lung melatonin levels. Melatonin synthesis in the lung reduced lipid peroxidation and increased PM2.5 engulfment and cell viability by activating high‐affinity melatonin receptors. Diesel exhaust particles (DEPs) promoted the synthesis of melatonin in a cultured cell line (RAW 264.7 cells) and rat alveolar macrophages via the expression of the gene encoding for AANAT through a mechanism dependent on activation of the NFκB pathway. Expression of the genes encoding AANAT, MT1, and MT2 was negatively correlated with cellular necroptosis, as disclosed by analysis of Gene Expression Omnibus (GEO) microarray data from the human alveolar macrophages of nonsmoking subjects. The enrichment score for antioxidant genes obtained from lung gene expression data (GTEx) was significantly correlated with the levels of AANAT and MT1 but not the MT2 melatonin receptor. Collectively, these data provide a systemic and mechanistic rationale for coordination of the pineal and extrapineal synthesis of melatonin by a standard damage‐associated stimulus, which activates the immune‐pineal axis and provides a new framework for understanding the effects of air pollution on lung diseases.</description><identifier>ISSN: 0742-3098</identifier><identifier>EISSN: 1600-079X</identifier><identifier>DOI: 10.1111/jpi.12636</identifier><identifier>PMID: 32043640</identifier><language>eng</language><publisher>England</publisher><subject>Air Pollution - adverse effects ; alveolar macrophages ; Animals ; Arylalkylamine N-Acetyltransferase - metabolism ; diesel particle ; Humans ; immune‐pineal axis ; Lung - metabolism ; Macrophages, Alveolar - metabolism ; Melatonin - metabolism ; NF‐kappa B ; Particulate Matter - adverse effects ; phagocytosis ; Pineal Gland - metabolism ; Rats ; Receptors, Melatonin - metabolism</subject><ispartof>Journal of pineal research, 2020-04, Vol.68 (3), p.e12636-n/a</ispartof><rights>2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2020 John Wiley & Sons A/S. 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Our goal was to show that PM2.5 eliciting a proinflammatory response activates the immune‐pineal axis, reducing the pineal synthesis and increasing the extrapineal synthesis of melatonin. Herein, we report that the exposure of rats to polluted air for 6 hours reduced nocturnal plasma melatonin levels and increased lung melatonin levels. Melatonin synthesis in the lung reduced lipid peroxidation and increased PM2.5 engulfment and cell viability by activating high‐affinity melatonin receptors. Diesel exhaust particles (DEPs) promoted the synthesis of melatonin in a cultured cell line (RAW 264.7 cells) and rat alveolar macrophages via the expression of the gene encoding for AANAT through a mechanism dependent on activation of the NFκB pathway. Expression of the genes encoding AANAT, MT1, and MT2 was negatively correlated with cellular necroptosis, as disclosed by analysis of Gene Expression Omnibus (GEO) microarray data from the human alveolar macrophages of nonsmoking subjects. The enrichment score for antioxidant genes obtained from lung gene expression data (GTEx) was significantly correlated with the levels of AANAT and MT1 but not the MT2 melatonin receptor. Collectively, these data provide a systemic and mechanistic rationale for coordination of the pineal and extrapineal synthesis of melatonin by a standard damage‐associated stimulus, which activates the immune‐pineal axis and provides a new framework for understanding the effects of air pollution on lung diseases.</description><subject>Air Pollution - adverse effects</subject><subject>alveolar macrophages</subject><subject>Animals</subject><subject>Arylalkylamine N-Acetyltransferase - metabolism</subject><subject>diesel particle</subject><subject>Humans</subject><subject>immune‐pineal axis</subject><subject>Lung - metabolism</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Melatonin - metabolism</subject><subject>NF‐kappa B</subject><subject>Particulate Matter - adverse effects</subject><subject>phagocytosis</subject><subject>Pineal Gland - metabolism</subject><subject>Rats</subject><subject>Receptors, Melatonin - metabolism</subject><issn>0742-3098</issn><issn>1600-079X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kL1OwzAQgC0EoqEw8ALIK0Pac3zxz4RQxU9RJRhAYotcx0WpkiayE9FuPALPyJMQCLBxy93w6ZPuI-SUwYT1M103xYQlgos9EjEBEIPUz_skAolJzEGrETkKYQ0ASilxSEY8AeQCISIX86rqNu7j7b0pNs6U1GyLQBtft862gXrT0rLbvATqtk0dXE7bmjZ1WXZtf5vCH5ODlSmDO_nZY_J0ffU4u40X9zfz2eUitjxJRWwR0Wq9lKnUK8BcQyK1YJhyichMapy2S6c0CIec5YI5yVCiU5hb5CrhY3I-eK2vQ_BulTW-qIzfZQyyrwhZHyH7jtCzZwPbdMvK5X_k79c9MB2A16J0u_9N2d3DfFB-Agk1ZfI</recordid><startdate>202004</startdate><enddate>202004</enddate><creator>Carvalho‐Sousa, Claudia Emanuele</creator><creator>Pereira, Eliana P.</creator><creator>Kinker, Gabriela S.</creator><creator>Veras, Mariana</creator><creator>Ferreira, Zulma S.</creator><creator>Barbosa‐Nunes, Fernanda P.</creator><creator>Martins, Joilson O.</creator><creator>Saldiva, Paulo H.N.</creator><creator>Reiter, Russel J.</creator><creator>Fernandes, Pedro A.</creator><creator>da Silveira Cruz‐Machado, Sanseray</creator><creator>Markus, Regina P.</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><orcidid>https://orcid.org/0000-0003-1676-442X</orcidid><orcidid>https://orcid.org/0000-0002-8363-4329</orcidid><orcidid>https://orcid.org/0000-0003-4606-6120</orcidid><orcidid>https://orcid.org/0000-0003-2005-8253</orcidid><orcidid>https://orcid.org/0000-0001-6571-837X</orcidid><orcidid>https://orcid.org/0000-0003-2630-7038</orcidid><orcidid>https://orcid.org/0000-0001-6763-4225</orcidid><orcidid>https://orcid.org/0000-0002-4871-8201</orcidid><orcidid>https://orcid.org/0000-0002-6937-7207</orcidid></search><sort><creationdate>202004</creationdate><title>Immune‐pineal axis protects rat lungs exposed to polluted air</title><author>Carvalho‐Sousa, Claudia Emanuele ; 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Our goal was to show that PM2.5 eliciting a proinflammatory response activates the immune‐pineal axis, reducing the pineal synthesis and increasing the extrapineal synthesis of melatonin. Herein, we report that the exposure of rats to polluted air for 6 hours reduced nocturnal plasma melatonin levels and increased lung melatonin levels. Melatonin synthesis in the lung reduced lipid peroxidation and increased PM2.5 engulfment and cell viability by activating high‐affinity melatonin receptors. Diesel exhaust particles (DEPs) promoted the synthesis of melatonin in a cultured cell line (RAW 264.7 cells) and rat alveolar macrophages via the expression of the gene encoding for AANAT through a mechanism dependent on activation of the NFκB pathway. Expression of the genes encoding AANAT, MT1, and MT2 was negatively correlated with cellular necroptosis, as disclosed by analysis of Gene Expression Omnibus (GEO) microarray data from the human alveolar macrophages of nonsmoking subjects. The enrichment score for antioxidant genes obtained from lung gene expression data (GTEx) was significantly correlated with the levels of AANAT and MT1 but not the MT2 melatonin receptor. Collectively, these data provide a systemic and mechanistic rationale for coordination of the pineal and extrapineal synthesis of melatonin by a standard damage‐associated stimulus, which activates the immune‐pineal axis and provides a new framework for understanding the effects of air pollution on lung diseases.</abstract><cop>England</cop><pmid>32043640</pmid><doi>10.1111/jpi.12636</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-1676-442X</orcidid><orcidid>https://orcid.org/0000-0002-8363-4329</orcidid><orcidid>https://orcid.org/0000-0003-4606-6120</orcidid><orcidid>https://orcid.org/0000-0003-2005-8253</orcidid><orcidid>https://orcid.org/0000-0001-6571-837X</orcidid><orcidid>https://orcid.org/0000-0003-2630-7038</orcidid><orcidid>https://orcid.org/0000-0001-6763-4225</orcidid><orcidid>https://orcid.org/0000-0002-4871-8201</orcidid><orcidid>https://orcid.org/0000-0002-6937-7207</orcidid></addata></record> |
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| identifier | ISSN: 0742-3098 |
| ispartof | Journal of pineal research, 2020-04, Vol.68 (3), p.e12636-n/a |
| issn | 0742-3098 1600-079X |
| language | eng |
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| source | Wiley-Blackwell Journals; MEDLINE |
| subjects | Air Pollution - adverse effects alveolar macrophages Animals Arylalkylamine N-Acetyltransferase - metabolism diesel particle Humans immune‐pineal axis Lung - metabolism Macrophages, Alveolar - metabolism Melatonin - metabolism NF‐kappa B Particulate Matter - adverse effects phagocytosis Pineal Gland - metabolism Rats Receptors, Melatonin - metabolism |
| title | Immune‐pineal axis protects rat lungs exposed to polluted air |
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