Dissection of host cell signal transduction during Acinetobacter baumannii-triggered inflammatory response
Infected airway epithelial cells up-regulate the expression of chemokines, chiefly IL-8, and antimicrobial molecules including beta-defensins (BD). Acinetobacter baumannii is a cause of hospital-acquired pneumonia. We examined whether A. baumannii induced the expressions of IL-8 and BD2 by airway ep...
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| creator | March, Catalina Regueiro, Verónica Llobet, Enrique Moranta, David Morey, Pau Garmendia, Junkal Bengoechea, José A |
| description | Infected airway epithelial cells up-regulate the expression of chemokines, chiefly IL-8, and antimicrobial molecules including beta-defensins (BD). Acinetobacter baumannii is a cause of hospital-acquired pneumonia. We examined whether A. baumannii induced the expressions of IL-8 and BD2 by airway epithelial cells and the receptors implicated in bacterial detection. A549 and human primary airway cells released IL-8 upon infection. A. baumannii-infected cells also increased the expression of BD2 which killed A. baummannii strains. IL-8 induction was via NF-kappaB and mitogen-activated kinases p38 and p44/42-dependent pathways. A. baumannii engaged Toll-like receptor (TLR) 2 and TLR4 pathways and A549 cells could use soluble CD14 as TLRs co-receptor. A. baumannii lipopolysaccharide stimulated IL-8 release by A549 cells and sCD14 facilitated the recognition of the lipopolysaccharide. Mass spectrometry analysis revealed that A. baumannii lipid A structure matches those with endotoxic potential. These results demonstrate that airway epithelial cells produce mediators important for A. baumannii clearance. |
| doi_str_mv | 10.1371/journal.pone.0010033 |
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Acinetobacter baumannii is a cause of hospital-acquired pneumonia. We examined whether A. baumannii induced the expressions of IL-8 and BD2 by airway epithelial cells and the receptors implicated in bacterial detection. A549 and human primary airway cells released IL-8 upon infection. A. baumannii-infected cells also increased the expression of BD2 which killed A. baummannii strains. IL-8 induction was via NF-kappaB and mitogen-activated kinases p38 and p44/42-dependent pathways. A. baumannii engaged Toll-like receptor (TLR) 2 and TLR4 pathways and A549 cells could use soluble CD14 as TLRs co-receptor. A. baumannii lipopolysaccharide stimulated IL-8 release by A549 cells and sCD14 facilitated the recognition of the lipopolysaccharide. Mass spectrometry analysis revealed that A. baumannii lipid A structure matches those with endotoxic potential. These results demonstrate that airway epithelial cells produce mediators important for A. baumannii clearance.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0010033</identifier><identifier>PMID: 20383325</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acinetobacter baumannii ; Acinetobacter baumannii - immunology ; Acinetobacter Infections ; Analysis ; Bacteria ; beta-Defensins - genetics ; CD14 antigen ; Cell Line ; Cellular signal transduction ; Chemokines ; Cytokines ; Defensins ; Dissection ; Epithelial Cells ; Health aspects ; Host-Pathogen Interactions ; Hostages ; Humans ; Immune system ; Immunology/Immunity to Infections ; Immunology/Innate Immunity ; Infection ; Inflammation ; Inflammation - etiology ; Inflammation Mediators - analysis ; Inflammatory response ; Interleukin 8 ; Interleukin-8 - genetics ; Kinases ; Lipid A ; Lipids ; Lipopolysaccharides ; Mass spectrometry ; Mass spectroscopy ; Microbiology/Cellular Microbiology and Pathogenesis ; Microbiology/Immunity to Infections ; Microbiology/Innate Immunity ; Mitogens ; Neutrophils ; NF-κB protein ; Nosocomial infections ; Pathogenesis ; Pathogens ; Pathways ; Peptides ; Pneumonia ; Pneumonia - immunology ; Pneumonia - microbiology ; Proteins ; Receptors ; Respiratory distress syndrome ; Respiratory System - cytology ; Respiratory tract ; Signal Transduction ; Surgery ; TLR4 protein ; Toll-like receptors ; Transduction ; Trends ; Up-Regulation - genetics</subject><ispartof>PloS one, 2010-04, Vol.5 (4), p.e10033-e10033</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 March et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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>March et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c757t-5517204ade9a17e9632d5094f4d60e6b7f34e119ddd5f08b8449fdc6055487183</citedby><cites>FETCH-LOGICAL-c757t-5517204ade9a17e9632d5094f4d60e6b7f34e119ddd5f08b8449fdc6055487183</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/PMC2850920/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2850920/$$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/20383325$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>March, Catalina</creatorcontrib><creatorcontrib>Regueiro, Verónica</creatorcontrib><creatorcontrib>Llobet, Enrique</creatorcontrib><creatorcontrib>Moranta, David</creatorcontrib><creatorcontrib>Morey, Pau</creatorcontrib><creatorcontrib>Garmendia, Junkal</creatorcontrib><creatorcontrib>Bengoechea, José A</creatorcontrib><title>Dissection of host cell signal transduction during Acinetobacter baumannii-triggered inflammatory response</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Infected airway epithelial cells up-regulate the expression of chemokines, chiefly IL-8, and antimicrobial molecules including beta-defensins (BD). Acinetobacter baumannii is a cause of hospital-acquired pneumonia. We examined whether A. baumannii induced the expressions of IL-8 and BD2 by airway epithelial cells and the receptors implicated in bacterial detection. A549 and human primary airway cells released IL-8 upon infection. A. baumannii-infected cells also increased the expression of BD2 which killed A. baummannii strains. IL-8 induction was via NF-kappaB and mitogen-activated kinases p38 and p44/42-dependent pathways. A. baumannii engaged Toll-like receptor (TLR) 2 and TLR4 pathways and A549 cells could use soluble CD14 as TLRs co-receptor. A. baumannii lipopolysaccharide stimulated IL-8 release by A549 cells and sCD14 facilitated the recognition of the lipopolysaccharide. Mass spectrometry analysis revealed that A. baumannii lipid A structure matches those with endotoxic potential. These results demonstrate that airway epithelial cells produce mediators important for A. baumannii clearance.</description><subject>Acinetobacter baumannii</subject><subject>Acinetobacter baumannii - immunology</subject><subject>Acinetobacter Infections</subject><subject>Analysis</subject><subject>Bacteria</subject><subject>beta-Defensins - genetics</subject><subject>CD14 antigen</subject><subject>Cell Line</subject><subject>Cellular signal transduction</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Defensins</subject><subject>Dissection</subject><subject>Epithelial Cells</subject><subject>Health aspects</subject><subject>Host-Pathogen Interactions</subject><subject>Hostages</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immunology/Immunity to Infections</subject><subject>Immunology/Innate Immunity</subject><subject>Infection</subject><subject>Inflammation</subject><subject>Inflammation - etiology</subject><subject>Inflammation Mediators - analysis</subject><subject>Inflammatory response</subject><subject>Interleukin 8</subject><subject>Interleukin-8 - genetics</subject><subject>Kinases</subject><subject>Lipid A</subject><subject>Lipids</subject><subject>Lipopolysaccharides</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Microbiology/Cellular Microbiology and Pathogenesis</subject><subject>Microbiology/Immunity to Infections</subject><subject>Microbiology/Innate Immunity</subject><subject>Mitogens</subject><subject>Neutrophils</subject><subject>NF-κB protein</subject><subject>Nosocomial infections</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Pathways</subject><subject>Peptides</subject><subject>Pneumonia</subject><subject>Pneumonia - immunology</subject><subject>Pneumonia - microbiology</subject><subject>Proteins</subject><subject>Receptors</subject><subject>Respiratory distress syndrome</subject><subject>Respiratory System - cytology</subject><subject>Respiratory tract</subject><subject>Signal Transduction</subject><subject>Surgery</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>Transduction</subject><subject>Trends</subject><subject>Up-Regulation - 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immunology</topic><topic>Acinetobacter Infections</topic><topic>Analysis</topic><topic>Bacteria</topic><topic>beta-Defensins - genetics</topic><topic>CD14 antigen</topic><topic>Cell Line</topic><topic>Cellular signal transduction</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Defensins</topic><topic>Dissection</topic><topic>Epithelial Cells</topic><topic>Health aspects</topic><topic>Host-Pathogen Interactions</topic><topic>Hostages</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immunology/Immunity to Infections</topic><topic>Immunology/Innate Immunity</topic><topic>Infection</topic><topic>Inflammation</topic><topic>Inflammation - etiology</topic><topic>Inflammation Mediators - analysis</topic><topic>Inflammatory response</topic><topic>Interleukin 8</topic><topic>Interleukin-8 - genetics</topic><topic>Kinases</topic><topic>Lipid A</topic><topic>Lipids</topic><topic>Lipopolysaccharides</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Microbiology/Cellular Microbiology and Pathogenesis</topic><topic>Microbiology/Immunity to Infections</topic><topic>Microbiology/Innate Immunity</topic><topic>Mitogens</topic><topic>Neutrophils</topic><topic>NF-κB protein</topic><topic>Nosocomial infections</topic><topic>Pathogenesis</topic><topic>Pathogens</topic><topic>Pathways</topic><topic>Peptides</topic><topic>Pneumonia</topic><topic>Pneumonia - 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Acinetobacter baumannii is a cause of hospital-acquired pneumonia. We examined whether A. baumannii induced the expressions of IL-8 and BD2 by airway epithelial cells and the receptors implicated in bacterial detection. A549 and human primary airway cells released IL-8 upon infection. A. baumannii-infected cells also increased the expression of BD2 which killed A. baummannii strains. IL-8 induction was via NF-kappaB and mitogen-activated kinases p38 and p44/42-dependent pathways. A. baumannii engaged Toll-like receptor (TLR) 2 and TLR4 pathways and A549 cells could use soluble CD14 as TLRs co-receptor. A. baumannii lipopolysaccharide stimulated IL-8 release by A549 cells and sCD14 facilitated the recognition of the lipopolysaccharide. Mass spectrometry analysis revealed that A. baumannii lipid A structure matches those with endotoxic potential. These results demonstrate that airway epithelial cells produce mediators important for A. baumannii clearance.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>20383325</pmid><doi>10.1371/journal.pone.0010033</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Acinetobacter baumannii Acinetobacter baumannii - immunology Acinetobacter Infections Analysis Bacteria beta-Defensins - genetics CD14 antigen Cell Line Cellular signal transduction Chemokines Cytokines Defensins Dissection Epithelial Cells Health aspects Host-Pathogen Interactions Hostages Humans Immune system Immunology/Immunity to Infections Immunology/Innate Immunity Infection Inflammation Inflammation - etiology Inflammation Mediators - analysis Inflammatory response Interleukin 8 Interleukin-8 - genetics Kinases Lipid A Lipids Lipopolysaccharides Mass spectrometry Mass spectroscopy Microbiology/Cellular Microbiology and Pathogenesis Microbiology/Immunity to Infections Microbiology/Innate Immunity Mitogens Neutrophils NF-κB protein Nosocomial infections Pathogenesis Pathogens Pathways Peptides Pneumonia Pneumonia - immunology Pneumonia - microbiology Proteins Receptors Respiratory distress syndrome Respiratory System - cytology Respiratory tract Signal Transduction Surgery TLR4 protein Toll-like receptors Transduction Trends Up-Regulation - genetics |
| title | Dissection of host cell signal transduction during Acinetobacter baumannii-triggered inflammatory response |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T06%3A40%3A28IST&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=Dissection%20of%20host%20cell%20signal%20transduction%20during%20Acinetobacter%20baumannii-triggered%20inflammatory%20response&rft.jtitle=PloS%20one&rft.au=March,%20Catalina&rft.date=2010-04-07&rft.volume=5&rft.issue=4&rft.spage=e10033&rft.epage=e10033&rft.pages=e10033-e10033&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0010033&rft_dat=%3Cgale_plos_%3EA473905655%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=1289443876&rft_id=info:pmid/20383325&rft_galeid=A473905655&rft_doaj_id=oai_doaj_org_article_e0d1fef187c54f84b21e9cbbdb1cab36&rfr_iscdi=true |