CCL20 and Beta-Defensin 2 Production by Human Lung Epithelial Cells and Macrophages in Response to Brucella abortus Infection
Both CCL20 and human β-defensin 2 (hBD2) interact with the same membrane receptor and display chemotactic and antimicrobial activities. They are produced by airway epithelia in response to infectious agents and proinflammatory cytokines. Whereas Brucella spp. can infect humans through inhalation, th...
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| Veröffentlicht in: | PloS one 2015-10, Vol.10 (10), p.e0140408-e0140408 |
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| description | Both CCL20 and human β-defensin 2 (hBD2) interact with the same membrane receptor and display chemotactic and antimicrobial activities. They are produced by airway epithelia in response to infectious agents and proinflammatory cytokines. Whereas Brucella spp. can infect humans through inhalation, their ability to induce CCL20 and hBD2 in lung cells is unknown. Here we show that B. abortus induces CCL20 expression in human alveolar (A549) or bronchial (Calu-6) epithelial cell lines, primary alveolar epithelial cells, primary human monocytes, monocyte-derived macrophages and the monocytic cell line THP-1. CCL20 expression was mainly mediated by JNK1/2 and NF-kB in both Calu-6 and THP-1 cells. CCL20 secretion was markedly induced in A549, Calu-6 and THP-1 cells by heat-killed B. abortus or a model Brucella lipoprotein (L-Omp19) but not by the B. abortus lipopolysaccharide (LPS). Accordingly, CCL20 production by B. abortus-infected cells was strongly TLR2-dependent. Whereas hBD2 expression was not induced by B. abortus infection, it was significantly induced in A549 cells by conditioned media from B. abortus-infected THP-1 monocytes (CMB). A similar inducing effect was observed on CCL20 secretion. Experiments using blocking agents revealed that IL-1β, but not TNF-α, was involved in the induction of hBD2 and CCL20 secretion by CMB. In the in vitro antimicrobial assay, the lethal dose (LD) 50 of CCL20 for B. abortus (>50 μg/ml) was markedly higher than that against E. coli (1.5 μg/ml) or a B. abortus mutant lacking the O polysaccharide in its LPS (8.7 ug/ml). hBD2 did not kill any of the B. abortus strains at the tested concentrations. These results show that human lung epithelial cells secrete CCL20 and hBD2 in response to B. abortus and/or to cytokines produced by infected monocytes. Whereas these molecules do not seem to exert antimicrobial activity against this pathogen, they could recruit immune cells to the infection site. |
| doi_str_mv | 10.1371/journal.pone.0140408 |
| format | Article |
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They are produced by airway epithelia in response to infectious agents and proinflammatory cytokines. Whereas Brucella spp. can infect humans through inhalation, their ability to induce CCL20 and hBD2 in lung cells is unknown. Here we show that B. abortus induces CCL20 expression in human alveolar (A549) or bronchial (Calu-6) epithelial cell lines, primary alveolar epithelial cells, primary human monocytes, monocyte-derived macrophages and the monocytic cell line THP-1. CCL20 expression was mainly mediated by JNK1/2 and NF-kB in both Calu-6 and THP-1 cells. CCL20 secretion was markedly induced in A549, Calu-6 and THP-1 cells by heat-killed B. abortus or a model Brucella lipoprotein (L-Omp19) but not by the B. abortus lipopolysaccharide (LPS). Accordingly, CCL20 production by B. abortus-infected cells was strongly TLR2-dependent. Whereas hBD2 expression was not induced by B. abortus infection, it was significantly induced in A549 cells by conditioned media from B. abortus-infected THP-1 monocytes (CMB). A similar inducing effect was observed on CCL20 secretion. Experiments using blocking agents revealed that IL-1β, but not TNF-α, was involved in the induction of hBD2 and CCL20 secretion by CMB. In the in vitro antimicrobial assay, the lethal dose (LD) 50 of CCL20 for B. abortus (>50 μg/ml) was markedly higher than that against E. coli (1.5 μg/ml) or a B. abortus mutant lacking the O polysaccharide in its LPS (8.7 ug/ml). hBD2 did not kill any of the B. abortus strains at the tested concentrations. These results show that human lung epithelial cells secrete CCL20 and hBD2 in response to B. abortus and/or to cytokines produced by infected monocytes. Whereas these molecules do not seem to exert antimicrobial activity against this pathogen, they could recruit immune cells to the infection site.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0140408</identifier><identifier>PMID: 26448160</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alveolar Epithelial Cells - metabolism ; Alveolar Epithelial Cells - microbiology ; Alveolar Epithelial Cells - secretion ; Alveoli ; Anti-Bacterial Agents - pharmacology ; Antiinfectives and antibacterials ; Antimicrobial activity ; Antimicrobial agents ; Bacteria ; beta-Defensins - biosynthesis ; beta-Defensins - pharmacology ; beta-Defensins - secretion ; Brucella ; Brucella abortus ; Brucella abortus - immunology ; Brucellosis ; Brucellosis - immunology ; Brucellosis - metabolism ; Brucellosis - microbiology ; Care and treatment ; CCL20 protein ; Cell Line ; Cell Line, Tumor ; Cell lines ; Chemokine CCL20 - biosynthesis ; Chemokine CCL20 - pharmacology ; Chemokine CCL20 - secretion ; Chemokines ; Conditioning ; Cytokines ; Dendritic cells ; Diagnosis ; E coli ; Epithelial cells ; Escherichia coli ; Gram-positive bacteria ; Health aspects ; Humans ; IL-1β ; Immune system ; Immunity, Innate ; Infections ; Inflammation ; Inhalation ; JNK protein ; Klebsiella pneumoniae ; Lethal dose ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; Lung - immunology ; Lung - microbiology ; Lung - pathology ; Lungs ; Lymphocytes B ; Macrophages ; MAP Kinase Signaling System ; Microbial Sensitivity Tests ; Monocytes ; Monocytes - immunology ; Monocytes - metabolism ; Monocytes - microbiology ; NF-κB protein ; Outer membrane proteins ; Pathogens ; Peptides ; Polysaccharides ; Respiration ; Respiratory tract ; Risk factors ; Rodents ; TLR2 protein ; Toll-Like Receptor 2 - metabolism ; Toll-like receptors ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2015-10, Vol.10 (10), p.e0140408-e0140408</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Hielpos 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 Hielpos et al 2015 Hielpos et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-4e2ab58cb2d60851eee1274048cdbb924d9bf7f6c6b7d105adad43a2dfadcf3b3</citedby><cites>FETCH-LOGICAL-c692t-4e2ab58cb2d60851eee1274048cdbb924d9bf7f6c6b7d105adad43a2dfadcf3b3</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/PMC4598116/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598116/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26448160$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hielpos, M Soledad</creatorcontrib><creatorcontrib>Ferrero, Mariana C</creatorcontrib><creatorcontrib>Fernández, Andrea G</creatorcontrib><creatorcontrib>Bonetto, Josefina</creatorcontrib><creatorcontrib>Giambartolomei, Guillermo H</creatorcontrib><creatorcontrib>Fossati, Carlos A</creatorcontrib><creatorcontrib>Baldi, Pablo C</creatorcontrib><title>CCL20 and Beta-Defensin 2 Production by Human Lung Epithelial Cells and Macrophages in Response to Brucella abortus Infection</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Both CCL20 and human β-defensin 2 (hBD2) interact with the same membrane receptor and display chemotactic and antimicrobial activities. They are produced by airway epithelia in response to infectious agents and proinflammatory cytokines. Whereas Brucella spp. can infect humans through inhalation, their ability to induce CCL20 and hBD2 in lung cells is unknown. Here we show that B. abortus induces CCL20 expression in human alveolar (A549) or bronchial (Calu-6) epithelial cell lines, primary alveolar epithelial cells, primary human monocytes, monocyte-derived macrophages and the monocytic cell line THP-1. CCL20 expression was mainly mediated by JNK1/2 and NF-kB in both Calu-6 and THP-1 cells. CCL20 secretion was markedly induced in A549, Calu-6 and THP-1 cells by heat-killed B. abortus or a model Brucella lipoprotein (L-Omp19) but not by the B. abortus lipopolysaccharide (LPS). Accordingly, CCL20 production by B. abortus-infected cells was strongly TLR2-dependent. Whereas hBD2 expression was not induced by B. abortus infection, it was significantly induced in A549 cells by conditioned media from B. abortus-infected THP-1 monocytes (CMB). A similar inducing effect was observed on CCL20 secretion. Experiments using blocking agents revealed that IL-1β, but not TNF-α, was involved in the induction of hBD2 and CCL20 secretion by CMB. In the in vitro antimicrobial assay, the lethal dose (LD) 50 of CCL20 for B. abortus (>50 μg/ml) was markedly higher than that against E. coli (1.5 μg/ml) or a B. abortus mutant lacking the O polysaccharide in its LPS (8.7 ug/ml). hBD2 did not kill any of the B. abortus strains at the tested concentrations. These results show that human lung epithelial cells secrete CCL20 and hBD2 in response to B. abortus and/or to cytokines produced by infected monocytes. Whereas these molecules do not seem to exert antimicrobial activity against this pathogen, they could recruit immune cells to the infection site.</description><subject>Alveolar Epithelial Cells - metabolism</subject><subject>Alveolar Epithelial Cells - microbiology</subject><subject>Alveolar Epithelial Cells - secretion</subject><subject>Alveoli</subject><subject>Anti-Bacterial Agents - pharmacology</subject><subject>Antiinfectives and antibacterials</subject><subject>Antimicrobial activity</subject><subject>Antimicrobial agents</subject><subject>Bacteria</subject><subject>beta-Defensins - biosynthesis</subject><subject>beta-Defensins - pharmacology</subject><subject>beta-Defensins - secretion</subject><subject>Brucella</subject><subject>Brucella abortus</subject><subject>Brucella abortus - immunology</subject><subject>Brucellosis</subject><subject>Brucellosis - immunology</subject><subject>Brucellosis - metabolism</subject><subject>Brucellosis - microbiology</subject><subject>Care and treatment</subject><subject>CCL20 protein</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell lines</subject><subject>Chemokine CCL20 - biosynthesis</subject><subject>Chemokine CCL20 - pharmacology</subject><subject>Chemokine CCL20 - secretion</subject><subject>Chemokines</subject><subject>Conditioning</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Diagnosis</subject><subject>E coli</subject><subject>Epithelial cells</subject><subject>Escherichia coli</subject><subject>Gram-positive bacteria</subject><subject>Health aspects</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Immune system</subject><subject>Immunity, Innate</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Inhalation</subject><subject>JNK protein</subject><subject>Klebsiella pneumoniae</subject><subject>Lethal dose</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Lung - immunology</subject><subject>Lung - microbiology</subject><subject>Lung - pathology</subject><subject>Lungs</subject><subject>Lymphocytes B</subject><subject>Macrophages</subject><subject>MAP Kinase Signaling System</subject><subject>Microbial Sensitivity Tests</subject><subject>Monocytes</subject><subject>Monocytes - immunology</subject><subject>Monocytes - metabolism</subject><subject>Monocytes - microbiology</subject><subject>NF-κB protein</subject><subject>Outer membrane proteins</subject><subject>Pathogens</subject><subject>Peptides</subject><subject>Polysaccharides</subject><subject>Respiration</subject><subject>Respiratory tract</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>TLR2 protein</subject><subject>Toll-Like Receptor 2 - metabolism</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor-α</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>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYqPwDxBYQkJw0eKvOMkN0lYGq1Q0ND5uLTs-SV2ldokTxC7477htNjVoFygXiU6e97XPa58keU7wjLCMvFv7vnWqmW29gxkmHHOcP0hOScHoVFDMHh59nyRPQlhjnLJciMfJCRWc50Tg0-TPfL6kGCln0Dl0avoBKnDBOkTRl9abvuysd0jfoMt-oxxa9q5GF1vbraCxqkFzaJqwV39WZeu3K1VDQFF-DSFuLADqPDpv-zJyCint264PaOEq2Bs_TR5VqgnwbHhPku8fL77NL6fLq0-L-dlyWoqCdlMOVOk0LzU1AucpAQBCs9hxXhqtC8pNoausEqXQmSE4VUYZzhQ1lTJlxTSbJC8PvtvGBzkkFyTJKI4ZpTiPxOJAGK_WctvajWpvpFdW7gu-raVqO1s2IDUmlOesEEQxrllWaCgYFlQbQ_muMkneD6v1egOmBNe1qhmZjv84u5K1_yV5WuSEiGjwZjBo_c8eQic3NuwjdOD7_b4J43keT3aSvPoHvb-7gapVbMC6ysd1y52pPOMsJsYFo5Ga3UPFx8DGlvGaVTbWR4K3I0FkOvjd1aoPQS6-Xv8_e_VjzL4-Ylegmm4VfNPvrkwYg_wAxrsXQgvVXcgEy92U3KYhd1MihymJshfHB3Qnuh0L9hcKZwwj</recordid><startdate>20151008</startdate><enddate>20151008</enddate><creator>Hielpos, M Soledad</creator><creator>Ferrero, Mariana C</creator><creator>Fernández, Andrea G</creator><creator>Bonetto, Josefina</creator><creator>Giambartolomei, Guillermo H</creator><creator>Fossati, Carlos A</creator><creator>Baldi, Pablo C</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>AEUYN</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>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20151008</creationdate><title>CCL20 and Beta-Defensin 2 Production by Human Lung Epithelial Cells and Macrophages in Response to Brucella abortus Infection</title><author>Hielpos, M Soledad ; Ferrero, Mariana C ; Fernández, Andrea G ; Bonetto, Josefina ; Giambartolomei, Guillermo H ; Fossati, Carlos A ; Baldi, Pablo C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-4e2ab58cb2d60851eee1274048cdbb924d9bf7f6c6b7d105adad43a2dfadcf3b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Alveolar Epithelial Cells - 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pharmacology</topic><topic>Lung - immunology</topic><topic>Lung - microbiology</topic><topic>Lung - pathology</topic><topic>Lungs</topic><topic>Lymphocytes B</topic><topic>Macrophages</topic><topic>MAP Kinase Signaling System</topic><topic>Microbial Sensitivity Tests</topic><topic>Monocytes</topic><topic>Monocytes - immunology</topic><topic>Monocytes - metabolism</topic><topic>Monocytes - microbiology</topic><topic>NF-κB protein</topic><topic>Outer membrane proteins</topic><topic>Pathogens</topic><topic>Peptides</topic><topic>Polysaccharides</topic><topic>Respiration</topic><topic>Respiratory tract</topic><topic>Risk factors</topic><topic>Rodents</topic><topic>TLR2 protein</topic><topic>Toll-Like Receptor 2 - metabolism</topic><topic>Toll-like receptors</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hielpos, M Soledad</creatorcontrib><creatorcontrib>Ferrero, Mariana C</creatorcontrib><creatorcontrib>Fernández, Andrea G</creatorcontrib><creatorcontrib>Bonetto, Josefina</creatorcontrib><creatorcontrib>Giambartolomei, Guillermo H</creatorcontrib><creatorcontrib>Fossati, Carlos A</creatorcontrib><creatorcontrib>Baldi, Pablo C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hielpos, M Soledad</au><au>Ferrero, Mariana C</au><au>Fernández, Andrea G</au><au>Bonetto, Josefina</au><au>Giambartolomei, Guillermo H</au><au>Fossati, Carlos A</au><au>Baldi, Pablo C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CCL20 and Beta-Defensin 2 Production by Human Lung Epithelial Cells and Macrophages in Response to Brucella abortus Infection</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-10-08</date><risdate>2015</risdate><volume>10</volume><issue>10</issue><spage>e0140408</spage><epage>e0140408</epage><pages>e0140408-e0140408</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Both CCL20 and human β-defensin 2 (hBD2) interact with the same membrane receptor and display chemotactic and antimicrobial activities. They are produced by airway epithelia in response to infectious agents and proinflammatory cytokines. Whereas Brucella spp. can infect humans through inhalation, their ability to induce CCL20 and hBD2 in lung cells is unknown. Here we show that B. abortus induces CCL20 expression in human alveolar (A549) or bronchial (Calu-6) epithelial cell lines, primary alveolar epithelial cells, primary human monocytes, monocyte-derived macrophages and the monocytic cell line THP-1. CCL20 expression was mainly mediated by JNK1/2 and NF-kB in both Calu-6 and THP-1 cells. CCL20 secretion was markedly induced in A549, Calu-6 and THP-1 cells by heat-killed B. abortus or a model Brucella lipoprotein (L-Omp19) but not by the B. abortus lipopolysaccharide (LPS). Accordingly, CCL20 production by B. abortus-infected cells was strongly TLR2-dependent. Whereas hBD2 expression was not induced by B. abortus infection, it was significantly induced in A549 cells by conditioned media from B. abortus-infected THP-1 monocytes (CMB). A similar inducing effect was observed on CCL20 secretion. Experiments using blocking agents revealed that IL-1β, but not TNF-α, was involved in the induction of hBD2 and CCL20 secretion by CMB. In the in vitro antimicrobial assay, the lethal dose (LD) 50 of CCL20 for B. abortus (>50 μg/ml) was markedly higher than that against E. coli (1.5 μg/ml) or a B. abortus mutant lacking the O polysaccharide in its LPS (8.7 ug/ml). hBD2 did not kill any of the B. abortus strains at the tested concentrations. These results show that human lung epithelial cells secrete CCL20 and hBD2 in response to B. abortus and/or to cytokines produced by infected monocytes. Whereas these molecules do not seem to exert antimicrobial activity against this pathogen, they could recruit immune cells to the infection site.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26448160</pmid><doi>10.1371/journal.pone.0140408</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2015-10, Vol.10 (10), p.e0140408-e0140408 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1720193508 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Alveolar Epithelial Cells - metabolism Alveolar Epithelial Cells - microbiology Alveolar Epithelial Cells - secretion Alveoli Anti-Bacterial Agents - pharmacology Antiinfectives and antibacterials Antimicrobial activity Antimicrobial agents Bacteria beta-Defensins - biosynthesis beta-Defensins - pharmacology beta-Defensins - secretion Brucella Brucella abortus Brucella abortus - immunology Brucellosis Brucellosis - immunology Brucellosis - metabolism Brucellosis - microbiology Care and treatment CCL20 protein Cell Line Cell Line, Tumor Cell lines Chemokine CCL20 - biosynthesis Chemokine CCL20 - pharmacology Chemokine CCL20 - secretion Chemokines Conditioning Cytokines Dendritic cells Diagnosis E coli Epithelial cells Escherichia coli Gram-positive bacteria Health aspects Humans IL-1β Immune system Immunity, Innate Infections Inflammation Inhalation JNK protein Klebsiella pneumoniae Lethal dose Lipopolysaccharides Lipopolysaccharides - pharmacology Lung - immunology Lung - microbiology Lung - pathology Lungs Lymphocytes B Macrophages MAP Kinase Signaling System Microbial Sensitivity Tests Monocytes Monocytes - immunology Monocytes - metabolism Monocytes - microbiology NF-κB protein Outer membrane proteins Pathogens Peptides Polysaccharides Respiration Respiratory tract Risk factors Rodents TLR2 protein Toll-Like Receptor 2 - metabolism Toll-like receptors Tumor necrosis factor-α |
| title | CCL20 and Beta-Defensin 2 Production by Human Lung Epithelial Cells and Macrophages in Response to Brucella abortus Infection |
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