Transcriptomic Analyses of the Biological Effects of Airborne PM2.5 Exposure on Human Bronchial Epithelial Cells
Epidemiological studies have associated high levels of airborne particulate matter (PM) with increased respiratory diseases. In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of par...
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| creator | Zhou, Zhixiang Liu, Yanghua Duan, Fengkui Qin, Mengnan Wu, Fengchang Sheng, Wang Yang, Lixin Liu, Jianguo He, Kebin |
| description | Epidemiological studies have associated high levels of airborne particulate matter (PM) with increased respiratory diseases. In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of particles smaller than 2.5 μm (PM2.5) collected from Beijing, China. After observing that PM2.5 decreased cell viability in a dose-dependent manner, we first used Illumina RNA-seq to identify genes and pathways that may contribute to PM2.5-induced toxicity to 16HBE cells. A total of 539 genes, 283 up-regulated and 256 down-regulated, were identified to be significantly differentially expressed after exposure to 25 μg/cm2 PM2.5. PM2.5 induced a large number of genes involved in responses to xenobtiotic stimuli, metabolic response, and inflammatory and immune response pathways such as MAPK signaling and cytokine-cytokine receptor interaction, which might contribute to PM2.5-related pulmonary diseases. We then confirmed our RNA-seq results by qPCR and by analysis of IL-6, CYP1A1, and IL-8 protein expression. Finally, ELISA assay demonstrated a significant association between exposure to PM2.5 and secretion of IL-6. This research provides a new insight into the mechanisms underlying PM2.5-induced respiratory diseases in Beijing. |
| doi_str_mv | 10.1371/journal.pone.0138267 |
| format | Article |
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In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of particles smaller than 2.5 μm (PM2.5) collected from Beijing, China. After observing that PM2.5 decreased cell viability in a dose-dependent manner, we first used Illumina RNA-seq to identify genes and pathways that may contribute to PM2.5-induced toxicity to 16HBE cells. A total of 539 genes, 283 up-regulated and 256 down-regulated, were identified to be significantly differentially expressed after exposure to 25 μg/cm2 PM2.5. PM2.5 induced a large number of genes involved in responses to xenobtiotic stimuli, metabolic response, and inflammatory and immune response pathways such as MAPK signaling and cytokine-cytokine receptor interaction, which might contribute to PM2.5-related pulmonary diseases. We then confirmed our RNA-seq results by qPCR and by analysis of IL-6, CYP1A1, and IL-8 protein expression. Finally, ELISA assay demonstrated a significant association between exposure to PM2.5 and secretion of IL-6. This research provides a new insight into the mechanisms underlying PM2.5-induced respiratory diseases in Beijing.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0138267</identifier><identifier>PMID: 26382838</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Air Pollutants - pharmacology ; Air pollution ; Airborne particulates ; Bioengineering ; Biological effects ; Bronchi - cytology ; Bronchi - drug effects ; Bronchi - metabolism ; Cells, Cultured ; China ; Cytochrome P450 ; Cytokines ; Environmental science ; Enzyme-linked immunosorbent assay ; Epidemiology ; Epithelial cells ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Exposure ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation - drug effects ; Genes ; Humans ; Immune response ; Immune system ; Inflammation ; Inhalation Exposure - analysis ; Interleukin 6 ; Interleukin 8 ; Laboratories ; Life sciences ; Lung diseases ; MAP kinase ; Metabolic response ; Outdoor air quality ; Oxidative stress ; Particulate emissions ; Particulate matter ; Particulate Matter - pharmacology ; Pollutants ; Reactive Oxygen Species - metabolism ; Respiratory diseases ; Respiratory Mucosa - cytology ; Respiratory Mucosa - drug effects ; Respiratory Mucosa - metabolism ; Ribonucleic acid ; RNA ; Toxicity ; Toxicology ; Transcriptome - drug effects</subject><ispartof>PloS one, 2015-09, Vol.10 (9), p.e0138267</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Zhou et al 2015 Zhou et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-dbd00de6fb4499aeb8f03b3c0f3657cb9ac94778a28584da3535bf11db575f3a3</citedby><cites>FETCH-LOGICAL-c692t-dbd00de6fb4499aeb8f03b3c0f3657cb9ac94778a28584da3535bf11db575f3a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575100/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575100/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26382838$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zheng, Song Guo</contributor><creatorcontrib>Zhou, Zhixiang</creatorcontrib><creatorcontrib>Liu, Yanghua</creatorcontrib><creatorcontrib>Duan, Fengkui</creatorcontrib><creatorcontrib>Qin, Mengnan</creatorcontrib><creatorcontrib>Wu, Fengchang</creatorcontrib><creatorcontrib>Sheng, Wang</creatorcontrib><creatorcontrib>Yang, Lixin</creatorcontrib><creatorcontrib>Liu, Jianguo</creatorcontrib><creatorcontrib>He, Kebin</creatorcontrib><title>Transcriptomic Analyses of the Biological Effects of Airborne PM2.5 Exposure on Human Bronchial Epithelial Cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Epidemiological studies have associated high levels of airborne particulate matter (PM) with increased respiratory diseases. In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of particles smaller than 2.5 μm (PM2.5) collected from Beijing, China. After observing that PM2.5 decreased cell viability in a dose-dependent manner, we first used Illumina RNA-seq to identify genes and pathways that may contribute to PM2.5-induced toxicity to 16HBE cells. A total of 539 genes, 283 up-regulated and 256 down-regulated, were identified to be significantly differentially expressed after exposure to 25 μg/cm2 PM2.5. PM2.5 induced a large number of genes involved in responses to xenobtiotic stimuli, metabolic response, and inflammatory and immune response pathways such as MAPK signaling and cytokine-cytokine receptor interaction, which might contribute to PM2.5-related pulmonary diseases. We then confirmed our RNA-seq results by qPCR and by analysis of IL-6, CYP1A1, and IL-8 protein expression. Finally, ELISA assay demonstrated a significant association between exposure to PM2.5 and secretion of IL-6. This research provides a new insight into the mechanisms underlying PM2.5-induced respiratory diseases in Beijing.</description><subject>Air Pollutants - pharmacology</subject><subject>Air pollution</subject><subject>Airborne particulates</subject><subject>Bioengineering</subject><subject>Biological effects</subject><subject>Bronchi - cytology</subject><subject>Bronchi - drug effects</subject><subject>Bronchi - metabolism</subject><subject>Cells, Cultured</subject><subject>China</subject><subject>Cytochrome P450</subject><subject>Cytokines</subject><subject>Environmental science</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Epidemiology</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Exposure</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Inhalation Exposure - analysis</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Laboratories</subject><subject>Life sciences</subject><subject>Lung diseases</subject><subject>MAP kinase</subject><subject>Metabolic response</subject><subject>Outdoor air quality</subject><subject>Oxidative stress</subject><subject>Particulate emissions</subject><subject>Particulate matter</subject><subject>Particulate Matter - pharmacology</subject><subject>Pollutants</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Respiratory diseases</subject><subject>Respiratory Mucosa - cytology</subject><subject>Respiratory Mucosa - drug effects</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Toxicity</subject><subject>Toxicology</subject><subject>Transcriptome - drug effects</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl9rFDEUxQdRbK1-A9EBQfBhx_ydmbwUtstqFyoVrb6GTCbZzZKdjElG2m9vtjstO6AgeUi4-Z2Ty83JstcQFBBX8OPWDb4TtuhdpwoAcY3K6kl2ChlGsxIB_PTofJK9CGELAMV1WT7PTlCZ8BrXp1l_40UXpDd9dDsj83myvAsq5E7ncaPyC-OsWxspbL7UWsl4fzM3vnG-U_nXL6ig-fK2d2HwKnddfjnsRJdfeNfJjdmrepN87P64UNaGl9kzLWxQr8b9LPvxaXmzuJxdXX9eLeZXM1kyFGdt0wLQqlI3hDAmVFNrgBssgcYlrWTDhGSkqmqBalqTVmCKaaMhbBtaUY0FPsveHnx76wIfhxU4rCBDNSMUJmJ1IFontrz3Zif8HXfC8PuC82sufDTSKl5LREiJoVKQEUUpg6yFLWEIUoYZksnrfHxtaHaqlaqLXtiJ6fSmMxu-dr85Se1CAJLBu9HAu1-DCvEfLY_UWqSuTKddMpM7EySfE8QAZazcexV_odJqVfriFBdtUn0i-DARJCaq27gWQwh89f3b_7PXP6fs-yN2o4SNm-DsEI3rwhQkB1B6F4JX-nFyEPB92h-mwfdp52Pak-zN8dQfRQ_xxn8AAvv5vg</recordid><startdate>20150918</startdate><enddate>20150918</enddate><creator>Zhou, Zhixiang</creator><creator>Liu, Yanghua</creator><creator>Duan, Fengkui</creator><creator>Qin, Mengnan</creator><creator>Wu, Fengchang</creator><creator>Sheng, Wang</creator><creator>Yang, Lixin</creator><creator>Liu, Jianguo</creator><creator>He, Kebin</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150918</creationdate><title>Transcriptomic Analyses of the Biological Effects of Airborne PM2.5 Exposure on Human Bronchial Epithelial Cells</title><author>Zhou, Zhixiang ; Liu, Yanghua ; Duan, Fengkui ; Qin, Mengnan ; Wu, Fengchang ; Sheng, Wang ; Yang, Lixin ; Liu, Jianguo ; He, Kebin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-dbd00de6fb4499aeb8f03b3c0f3657cb9ac94778a28584da3535bf11db575f3a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Air Pollutants - pharmacology</topic><topic>Air pollution</topic><topic>Airborne particulates</topic><topic>Bioengineering</topic><topic>Biological effects</topic><topic>Bronchi - cytology</topic><topic>Bronchi - drug effects</topic><topic>Bronchi - metabolism</topic><topic>Cells, Cultured</topic><topic>China</topic><topic>Cytochrome P450</topic><topic>Cytokines</topic><topic>Environmental science</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Epidemiology</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Exposure</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genes</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Inhalation Exposure - analysis</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Laboratories</topic><topic>Life sciences</topic><topic>Lung diseases</topic><topic>MAP kinase</topic><topic>Metabolic response</topic><topic>Outdoor air quality</topic><topic>Oxidative stress</topic><topic>Particulate emissions</topic><topic>Particulate matter</topic><topic>Particulate Matter - 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In order to investigate the mechanisms of air pollution-induced lung toxicity in humans, human bronchial epithelial cells (16HBE) were exposed to various concentrations of particles smaller than 2.5 μm (PM2.5) collected from Beijing, China. After observing that PM2.5 decreased cell viability in a dose-dependent manner, we first used Illumina RNA-seq to identify genes and pathways that may contribute to PM2.5-induced toxicity to 16HBE cells. A total of 539 genes, 283 up-regulated and 256 down-regulated, were identified to be significantly differentially expressed after exposure to 25 μg/cm2 PM2.5. PM2.5 induced a large number of genes involved in responses to xenobtiotic stimuli, metabolic response, and inflammatory and immune response pathways such as MAPK signaling and cytokine-cytokine receptor interaction, which might contribute to PM2.5-related pulmonary diseases. We then confirmed our RNA-seq results by qPCR and by analysis of IL-6, CYP1A1, and IL-8 protein expression. Finally, ELISA assay demonstrated a significant association between exposure to PM2.5 and secretion of IL-6. This research provides a new insight into the mechanisms underlying PM2.5-induced respiratory diseases in Beijing.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26382838</pmid><doi>10.1371/journal.pone.0138267</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Air Pollutants - pharmacology Air pollution Airborne particulates Bioengineering Biological effects Bronchi - cytology Bronchi - drug effects Bronchi - metabolism Cells, Cultured China Cytochrome P450 Cytokines Environmental science Enzyme-linked immunosorbent assay Epidemiology Epithelial cells Epithelial Cells - drug effects Epithelial Cells - metabolism Exposure Gene expression Gene Expression Profiling Gene Expression Regulation - drug effects Genes Humans Immune response Immune system Inflammation Inhalation Exposure - analysis Interleukin 6 Interleukin 8 Laboratories Life sciences Lung diseases MAP kinase Metabolic response Outdoor air quality Oxidative stress Particulate emissions Particulate matter Particulate Matter - pharmacology Pollutants Reactive Oxygen Species - metabolism Respiratory diseases Respiratory Mucosa - cytology Respiratory Mucosa - drug effects Respiratory Mucosa - metabolism Ribonucleic acid RNA Toxicity Toxicology Transcriptome - drug effects |
| title | Transcriptomic Analyses of the Biological Effects of Airborne PM2.5 Exposure on Human Bronchial Epithelial Cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T02%3A03%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Transcriptomic%20Analyses%20of%20the%20Biological%20Effects%20of%20Airborne%20PM2.5%20Exposure%20on%20Human%20Bronchial%20Epithelial%20Cells&rft.jtitle=PloS%20one&rft.au=Zhou,%20Zhixiang&rft.date=2015-09-18&rft.volume=10&rft.issue=9&rft.spage=e0138267&rft.pages=e0138267-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0138267&rft_dat=%3Cgale_plos_%3EA429059960%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1719289451&rft_id=info:pmid/26382838&rft_galeid=A429059960&rft_doaj_id=oai_doaj_org_article_8c244631ee194e55919d1d492159392c&rfr_iscdi=true |