Inhibition of Endothelial Interleukin-8 Production and Neutrophil Transmigration by Staphylococcus aureus Beta-Hemolysin
Neutrophils play a crucial role in the host response to infection with Staphylococcus aureus, which is a major human pathogen capable of causing life-threatening disease. Interleukin-8 (IL-8) is a potent chemoattractant and activator of neutrophils. We previously reported that S. aureus secretes a f...
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| Veröffentlicht in: | Infection and Immunity 2009-01, Vol.77 (1), p.327-334 |
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| creator | Tajima, Akiko Iwase, Tadayuki Shinji, Hitomi Seki, Keiko Mizunoe, Yoshimitsu |
| description | Neutrophils play a crucial role in the host response to infection with Staphylococcus aureus, which is a major human pathogen capable of causing life-threatening disease. Interleukin-8 (IL-8) is a potent chemoattractant and activator of neutrophils. We previously reported that S. aureus secretes a factor that suppresses IL-8 production by human endothelial cells. Here we isolated an inhibitor of IL-8 production from the supernatant and identified it as staphylococcal beta-hemolysin. Beta-hemolysin reduced IL-8 production without cytotoxicity to endothelial cells. Pretreatment with beta-hemolysin decreased the expression of both IL-8 mRNA and protein induced by tumor necrosis factor alpha (TNF-α). Migration of neutrophils across TNF-α-activated endothelium was also inhibited by beta-hemolysin. In contrast, beta-hemolysin had no effect on intercellular adhesive molecule 1 expression in activated endothelial cells. These results showed that beta-hemolysin produced by S. aureus interferes with inflammatory signaling in endothelial cells and may help S. aureus evade the host immune response. |
| doi_str_mv | 10.1128/IAI.00748-08 |
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Interleukin-8 (IL-8) is a potent chemoattractant and activator of neutrophils. We previously reported that S. aureus secretes a factor that suppresses IL-8 production by human endothelial cells. Here we isolated an inhibitor of IL-8 production from the supernatant and identified it as staphylococcal beta-hemolysin. Beta-hemolysin reduced IL-8 production without cytotoxicity to endothelial cells. Pretreatment with beta-hemolysin decreased the expression of both IL-8 mRNA and protein induced by tumor necrosis factor alpha (TNF-α). Migration of neutrophils across TNF-α-activated endothelium was also inhibited by beta-hemolysin. In contrast, beta-hemolysin had no effect on intercellular adhesive molecule 1 expression in activated endothelial cells. These results showed that beta-hemolysin produced by S. aureus interferes with inflammatory signaling in endothelial cells and may help S. aureus evade the host immune response.</description><identifier>ISSN: 0019-9567</identifier><identifier>EISSN: 1098-5522</identifier><identifier>DOI: 10.1128/IAI.00748-08</identifier><identifier>PMID: 18936175</identifier><identifier>CODEN: INFIBR</identifier><language>eng</language><publisher>Washington, DC: American Society for Microbiology</publisher><subject>Bacterial Toxins - toxicity ; Bacteriology ; Biological and medical sciences ; Cell adhesion ; Cell migration ; Cell Migration Assays, Leukocyte ; Cells, Cultured ; Cellular Microbiology: Pathogen-Host Cell Molecular Interactions ; Chemotactic factors ; Cytotoxicity ; Endothelial cells ; Endothelial Cells - microbiology ; Endothelium ; Fundamental and applied biological sciences. 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Psychology</subject><subject>Hemolysin Proteins - toxicity</subject><subject>Humans</subject><subject>Immune response</subject><subject>Infection</subject><subject>Inflammation</subject><subject>Interleukin 8</subject><subject>Interleukin-8 - antagonists & inhibitors</subject><subject>Leukocyte migration</subject><subject>Leukocytes (neutrophilic)</subject><subject>Microbiology</subject><subject>mRNA</subject><subject>Neutrophils - immunology</subject><subject>Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains</subject><subject>Pathogens</subject><subject>Signal transduction</subject><subject>Sphingomyelin Phosphodiesterase - toxicity</subject><subject>Staphylococcus aureus</subject><subject>Staphylococcus aureus - immunology</subject><subject>Tumor necrosis factor-a</subject><issn>0019-9567</issn><issn>1098-5522</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1v1DAQxSMEokvhxhlygRMpHjtOnAtSqQqNVAFS27M1cZyNwbEXOwH2v8f7oQIn5jIazU9PM-9l2XMgZwBUvG3P2zNC6lIURDzIVkAaUXBO6cNsRQg0RcOr-iR7EuPXNJZlKR5nJyAaVkHNV9mv1o2mM7PxLvdDful6P4_aGrR562YdrF6-GVeI_Evw_aL2HLo-_6SXOfjNaGx-G9DFyawD7rfdNr-ZcTNurVdeqSXmuASd2ns9Y3GlJ2-30bin2aMBbdTPjv00u_tweXtxVVx__thenF8XqhR8LijvFBk6LDnpOpWqgaovqwG7RgulBQOFuhuAIHZlMkHz9Boi40gZ03XNTrN3B93N0k26V9rNAa3cBDNh2EqPRv67cWaUa_9D0gooFZAEXh8Fgv--6DjLyUSlrUWn_RIlBdowyun_QcJEyeud4psDqIKPMejh_hogcpepTJnKfaaSiIS_-PuDP_AxxAS8OgIYFdoh5aFMvOcoQM2AlInLD9xo1uNPE7TEOEmTHKhrCZLRnVsvD8iAXuI6JJm7G0qAEUiX8wbYb85FwcU</recordid><startdate>20090101</startdate><enddate>20090101</enddate><creator>Tajima, Akiko</creator><creator>Iwase, Tadayuki</creator><creator>Shinji, Hitomi</creator><creator>Seki, Keiko</creator><creator>Mizunoe, Yoshimitsu</creator><general>American Society for Microbiology</general><general>American Society for Microbiology (ASM)</general><scope>FBQ</scope><scope>IQODW</scope><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>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>20090101</creationdate><title>Inhibition of Endothelial Interleukin-8 Production and Neutrophil Transmigration by Staphylococcus aureus Beta-Hemolysin</title><author>Tajima, Akiko ; Iwase, Tadayuki ; Shinji, Hitomi ; Seki, Keiko ; Mizunoe, Yoshimitsu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-25bc0fba450bbcccc916d46fab9e8ce831caebf10aab4748e5893aa35a233e773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Bacterial Toxins - toxicity</topic><topic>Bacteriology</topic><topic>Biological and medical sciences</topic><topic>Cell adhesion</topic><topic>Cell migration</topic><topic>Cell Migration Assays, Leukocyte</topic><topic>Cells, Cultured</topic><topic>Cellular Microbiology: Pathogen-Host Cell Molecular Interactions</topic><topic>Chemotactic factors</topic><topic>Cytotoxicity</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - microbiology</topic><topic>Endothelium</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hemolysin Proteins - toxicity</topic><topic>Humans</topic><topic>Immune response</topic><topic>Infection</topic><topic>Inflammation</topic><topic>Interleukin 8</topic><topic>Interleukin-8 - antagonists & inhibitors</topic><topic>Leukocyte migration</topic><topic>Leukocytes (neutrophilic)</topic><topic>Microbiology</topic><topic>mRNA</topic><topic>Neutrophils - immunology</topic><topic>Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains</topic><topic>Pathogens</topic><topic>Signal transduction</topic><topic>Sphingomyelin Phosphodiesterase - toxicity</topic><topic>Staphylococcus aureus</topic><topic>Staphylococcus aureus - immunology</topic><topic>Tumor necrosis factor-a</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tajima, Akiko</creatorcontrib><creatorcontrib>Iwase, Tadayuki</creatorcontrib><creatorcontrib>Shinji, Hitomi</creatorcontrib><creatorcontrib>Seki, Keiko</creatorcontrib><creatorcontrib>Mizunoe, Yoshimitsu</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Infection and Immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tajima, Akiko</au><au>Iwase, Tadayuki</au><au>Shinji, Hitomi</au><au>Seki, Keiko</au><au>Mizunoe, Yoshimitsu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Endothelial Interleukin-8 Production and Neutrophil Transmigration by Staphylococcus aureus Beta-Hemolysin</atitle><jtitle>Infection and Immunity</jtitle><addtitle>Infect Immun</addtitle><date>2009-01-01</date><risdate>2009</risdate><volume>77</volume><issue>1</issue><spage>327</spage><epage>334</epage><pages>327-334</pages><issn>0019-9567</issn><eissn>1098-5522</eissn><coden>INFIBR</coden><abstract>Neutrophils play a crucial role in the host response to infection with Staphylococcus aureus, which is a major human pathogen capable of causing life-threatening disease. Interleukin-8 (IL-8) is a potent chemoattractant and activator of neutrophils. We previously reported that S. aureus secretes a factor that suppresses IL-8 production by human endothelial cells. Here we isolated an inhibitor of IL-8 production from the supernatant and identified it as staphylococcal beta-hemolysin. Beta-hemolysin reduced IL-8 production without cytotoxicity to endothelial cells. Pretreatment with beta-hemolysin decreased the expression of both IL-8 mRNA and protein induced by tumor necrosis factor alpha (TNF-α). Migration of neutrophils across TNF-α-activated endothelium was also inhibited by beta-hemolysin. In contrast, beta-hemolysin had no effect on intercellular adhesive molecule 1 expression in activated endothelial cells. These results showed that beta-hemolysin produced by S. aureus interferes with inflammatory signaling in endothelial cells and may help S. aureus evade the host immune response.</abstract><cop>Washington, DC</cop><pub>American Society for Microbiology</pub><pmid>18936175</pmid><doi>10.1128/IAI.00748-08</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Bacterial Toxins - toxicity Bacteriology Biological and medical sciences Cell adhesion Cell migration Cell Migration Assays, Leukocyte Cells, Cultured Cellular Microbiology: Pathogen-Host Cell Molecular Interactions Chemotactic factors Cytotoxicity Endothelial cells Endothelial Cells - microbiology Endothelium Fundamental and applied biological sciences. Psychology Hemolysin Proteins - toxicity Humans Immune response Infection Inflammation Interleukin 8 Interleukin-8 - antagonists & inhibitors Leukocyte migration Leukocytes (neutrophilic) Microbiology mRNA Neutrophils - immunology Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains Pathogens Signal transduction Sphingomyelin Phosphodiesterase - toxicity Staphylococcus aureus Staphylococcus aureus - immunology Tumor necrosis factor-a |
| title | Inhibition of Endothelial Interleukin-8 Production and Neutrophil Transmigration by Staphylococcus aureus Beta-Hemolysin |
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