Exogenous Bovine Surfactant Suppresses Tumor Necrosis Factor-α Release by Murine Macrophages Stimulated by Genital Mycoplasmas
Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that appears to play a significant role in the development of neonatal chronic lung disease (CLD). Inflammation and CLD are also associated with respiratory tract colonization with genital mycoplasmas. The possible protective roles of sur...
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| Veröffentlicht in: | The Journal of infectious diseases 1998-10, Vol.178 (4), p.1122-1125 |
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| creator | Talati, Ajay J. Crouse, Dennis T. English, B. Keith Newman, Cynthia Livingston, Lisa Meals, Elizabeth |
| description | Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that appears to play a significant role in the development of neonatal chronic lung disease (CLD). Inflammation and CLD are also associated with respiratory tract colonization with genital mycoplasmas. The possible protective roles of surfactant in mitigating the inflammatory response to these microbes were investigated. Murine RAW 264.7 macrophages were preincubated with an exogenous surfactant and exposed overnight to sterile media, lipopolysaccharide (LPS), Mycoplasma hominis, or Ureaplasma urealyticum. Macrophages released TNF-α in response to challenge with LPS, U. urealyticum, and M. hominis in a concentration-dependent fashion. Surfactant suppressed LPS and M. hominis induced TNF-α production in a dose-dependent manner but suppressed U. urealyticum—mediated TNF-α production only at the higher dose tested. Similar effects were seen in hyperoxia (95% O2). Thus, exogenous bovine surfactant significantly inhibits the production of TNF-α by murine macrophages stimulated with genital mycoplasmas and bacterial LPS. |
| doi_str_mv | 10.1086/515695 |
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Surfactant suppressed LPS and M. hominis induced TNF-α production in a dose-dependent manner but suppressed U. urealyticum—mediated TNF-α production only at the higher dose tested. Similar effects were seen in hyperoxia (95% O2). Thus, exogenous bovine surfactant significantly inhibits the production of TNF-α by murine macrophages stimulated with genital mycoplasmas and bacterial LPS.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1086/515695</identifier><identifier>PMID: 9806043</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: The University of Chicago Press</publisher><subject>Analysis of the immune response. Humoral and cellular immunity ; Animals ; Biological and medical sciences ; Cattle ; Cytokines ; Drug Interactions ; Fundamental and applied biological sciences. 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Keith</creatorcontrib><creatorcontrib>Newman, Cynthia</creatorcontrib><creatorcontrib>Livingston, Lisa</creatorcontrib><creatorcontrib>Meals, Elizabeth</creatorcontrib><title>Exogenous Bovine Surfactant Suppresses Tumor Necrosis Factor-α Release by Murine Macrophages Stimulated by Genital Mycoplasmas</title><title>The Journal of infectious diseases</title><addtitle>The Journal of Infectious Diseases</addtitle><description>Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that appears to play a significant role in the development of neonatal chronic lung disease (CLD). Inflammation and CLD are also associated with respiratory tract colonization with genital mycoplasmas. The possible protective roles of surfactant in mitigating the inflammatory response to these microbes were investigated. Murine RAW 264.7 macrophages were preincubated with an exogenous surfactant and exposed overnight to sterile media, lipopolysaccharide (LPS), Mycoplasma hominis, or Ureaplasma urealyticum. Macrophages released TNF-α in response to challenge with LPS, U. urealyticum, and M. hominis in a concentration-dependent fashion. Surfactant suppressed LPS and M. hominis induced TNF-α production in a dose-dependent manner but suppressed U. urealyticum—mediated TNF-α production only at the higher dose tested. Similar effects were seen in hyperoxia (95% O2). Thus, exogenous bovine surfactant significantly inhibits the production of TNF-α by murine macrophages stimulated with genital mycoplasmas and bacterial LPS.</description><subject>Analysis of the immune response. Humoral and cellular immunity</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cattle</subject><subject>Cytokines</subject><subject>Drug Interactions</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Genitalia</subject><subject>Hyperoxia</subject><subject>Immunobiology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Lung diseases</subject><subject>Lung Diseases - immunology</subject><subject>Lung Diseases - microbiology</subject><subject>Lymphokines, interleukins ( function, expression)</subject><subject>Macrophages</subject><subject>Macrophages - cytology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - immunology</subject><subject>Major Articles</subject><subject>Mice</subject><subject>Mycoplasma</subject><subject>Mycoplasma hominis - immunology</subject><subject>Mycoplasmataceae - immunology</subject><subject>Pediatrics</subject><subject>Pulmonary Surfactants - pharmacology</subject><subject>Regulatory factors and their cellular receptors</subject><subject>Surfactants</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Ungulates</subject><subject>Ureaplasma - immunology</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtqGzEUhkVocRy3fYOCFiW7SXUZaUbLJOQGcWtqF0o2g2Z0JplkbujMBHuVZ-qL9JkiY-NupAPfp5-jn5AvnJ1xlurviitt1BGZciWTSGsuP5ApY0JEPDXmmJwgPjPGYqmTCZmYlOkwT8nb1bp7hLYbkV50r1ULdDn60haDbYcw9r0HREC6GpvO0x9Q-A4rpNfB6Hz07y_9BTVYBJpv6Hz024C5DVL_ZB_Ds-VQNWNtB3Bb4QbaarA1nW-Krq8tNhY_kY-lrRE-7-8Z-X19tbq8je5_3txdnt9HhTRqiArOylyXPFdOasWFdE5rwZwrAIzjPFGqtHkq4lTFShkjlBLhSCF2sS5Byhk53eVuP4Aeyqz3VWP9JuMs2xaY7QoM4ted2I95A-6g7RsL_NueWyxsXXrbFhUeNBHzRJr4f8wzhqIOWLKwK0914NGOVzjA-sCtf8l0IhOV3f55yKS8MGrBRbaQ7z7QkaA</recordid><startdate>19981001</startdate><enddate>19981001</enddate><creator>Talati, Ajay J.</creator><creator>Crouse, Dennis T.</creator><creator>English, B. 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Keith ; Newman, Cynthia ; Livingston, Lisa ; Meals, Elizabeth</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c395t-c10fb6f1b5d365123dd6620ddcee9d11755fab824854559925529258e4d46fe33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Analysis of the immune response. Humoral and cellular immunity</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cattle</topic><topic>Cytokines</topic><topic>Drug Interactions</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Genitalia</topic><topic>Hyperoxia</topic><topic>Immunobiology</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Lung diseases</topic><topic>Lung Diseases - immunology</topic><topic>Lung Diseases - microbiology</topic><topic>Lymphokines, interleukins ( function, expression)</topic><topic>Macrophages</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - immunology</topic><topic>Major Articles</topic><topic>Mice</topic><topic>Mycoplasma</topic><topic>Mycoplasma hominis - immunology</topic><topic>Mycoplasmataceae - immunology</topic><topic>Pediatrics</topic><topic>Pulmonary Surfactants - pharmacology</topic><topic>Regulatory factors and their cellular receptors</topic><topic>Surfactants</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Ungulates</topic><topic>Ureaplasma - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Talati, Ajay J.</creatorcontrib><creatorcontrib>Crouse, Dennis T.</creatorcontrib><creatorcontrib>English, B. Keith</creatorcontrib><creatorcontrib>Newman, Cynthia</creatorcontrib><creatorcontrib>Livingston, Lisa</creatorcontrib><creatorcontrib>Meals, Elizabeth</creatorcontrib><collection>Istex</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><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Talati, Ajay J.</au><au>Crouse, Dennis T.</au><au>English, B. Keith</au><au>Newman, Cynthia</au><au>Livingston, Lisa</au><au>Meals, Elizabeth</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exogenous Bovine Surfactant Suppresses Tumor Necrosis Factor-α Release by Murine Macrophages Stimulated by Genital Mycoplasmas</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>The Journal of Infectious Diseases</addtitle><date>1998-10-01</date><risdate>1998</risdate><volume>178</volume><issue>4</issue><spage>1122</spage><epage>1125</epage><pages>1122-1125</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that appears to play a significant role in the development of neonatal chronic lung disease (CLD). Inflammation and CLD are also associated with respiratory tract colonization with genital mycoplasmas. The possible protective roles of surfactant in mitigating the inflammatory response to these microbes were investigated. Murine RAW 264.7 macrophages were preincubated with an exogenous surfactant and exposed overnight to sterile media, lipopolysaccharide (LPS), Mycoplasma hominis, or Ureaplasma urealyticum. Macrophages released TNF-α in response to challenge with LPS, U. urealyticum, and M. hominis in a concentration-dependent fashion. Surfactant suppressed LPS and M. hominis induced TNF-α production in a dose-dependent manner but suppressed U. urealyticum—mediated TNF-α production only at the higher dose tested. Similar effects were seen in hyperoxia (95% O2). Thus, exogenous bovine surfactant significantly inhibits the production of TNF-α by murine macrophages stimulated with genital mycoplasmas and bacterial LPS.</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>9806043</pmid><doi>10.1086/515695</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| source | JSTOR Archive Collection A-Z Listing; Oxford University Press Journals All Titles (1996-Current); MEDLINE |
| subjects | Analysis of the immune response. Humoral and cellular immunity Animals Biological and medical sciences Cattle Cytokines Drug Interactions Fundamental and applied biological sciences. Psychology Fundamental immunology Genitalia Hyperoxia Immunobiology Lipopolysaccharides - pharmacology Lung diseases Lung Diseases - immunology Lung Diseases - microbiology Lymphokines, interleukins ( function, expression) Macrophages Macrophages - cytology Macrophages - drug effects Macrophages - immunology Major Articles Mice Mycoplasma Mycoplasma hominis - immunology Mycoplasmataceae - immunology Pediatrics Pulmonary Surfactants - pharmacology Regulatory factors and their cellular receptors Surfactants Tumor Necrosis Factor-alpha - biosynthesis Ungulates Ureaplasma - immunology |
| title | Exogenous Bovine Surfactant Suppresses Tumor Necrosis Factor-α Release by Murine Macrophages Stimulated by Genital Mycoplasmas |
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