Effect of influenza viras on phagocytic cells
Identifieur interne : 000627 ( Istex/Corpus ); précédent : 000626; suivant : 000628Effect of influenza viras on phagocytic cells
Auteurs : Y. Debets-Ossenkopp ; E. L. Mills ; W. C. Van Dijk ; H. A. Verbrugh ; J. VerhoefSource :
- European Journal of Clinical Microbiology [ 0722-2211 ] ; 1982-06-01.
English descriptors
- Teeft :
- Additional virus, Alveolar macrophages, Chemiluminescence, Chemotaxis, Control pmns, Influenza, Influenza infection, Influenza virus, Influenza virus particles, Influenza viruses, Leukocyte, Macrophage, Neuraminidase, Neutrophil, Phagocytic, Phagocytic cells, Phagocytic function, Phagocytosis, Pmns, Polymorphonuclear, Polymorphonuclear leukocytes, Staphylococcus aureus, Various concentrations, Vial, Virus, Virus particles, Virus suspension, Virus treatment, Water bath.
Abstract
Abstract: Many viral infections predispose to bacterial superinfection, and it has been suggested that the increased susceptibility to bacterial infections is at least in part due to the effect of virus on the phagocytic cell function. Since the mechanisms by which the viruses affect neutrophil function are not well understood, we studied the function of polymorphonuclear leukocytes (PMNs) after incubation with influenza virus. Phagocytosis was assayed by incubating influenza virus (strain type A-Texas-77 [H2N2]) treated leukocytes with3H-thymidine-labelled staphylococci. The oxidative metabolism of the PMNs was studied by measuring the chemiluminescence generated by virus-treated PMNs after incubation with zymosan. Chemotaxis was measured under agarose. After incubation with 107 EID50 units of influenza virus, PMNs ingested only 35 % of the bacteria, whereas control leukocytes ingested over 80 %. Influenza virus also reduced the mobility of the PMNs and markedly suppressed the generation of chemiluminiscence. UV-killed virus with intact neuraminidase produced similar effects but virus with heat-inactivated neuraminidase did not. Virus envelope-neuraminidase may be responsible for some of the effects of the virus on the PMNs.
Url:
DOI: 10.1007/BF02019619
Links to Exploration step
ISTEX:09BC710D957C6B17EB7C06F54AF9D98180C0B69FLe document en format XML
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Phagocytosis was assayed by incubating influenza virus (strain type A-Texas-77 [H2N2]) treated leukocytes with3H-thymidine-labelled staphylococci. The oxidative metabolism of the PMNs was studied by measuring the chemiluminescence generated by virus-treated PMNs after incubation with zymosan. Chemotaxis was measured under agarose. After incubation with 107 EID50 units of influenza virus, PMNs ingested only 35 % of the bacteria, whereas control leukocytes ingested over 80 %. Influenza virus also reduced the mobility of the PMNs and markedly suppressed the generation of chemiluminiscence. UV-killed virus with intact neuraminidase produced similar effects but virus with heat-inactivated neuraminidase did not. 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Since the mechanisms by which the viruses affect neutrophil function are not well understood, we studied the function of polymorphonuclear leukocytes (PMNs) after incubation with influenza virus. Phagocytosis was assayed by incubating influenza virus (strain type A-Texas-77 [H2N2]) treated leukocytes with3H-thymidine-labelled staphylococci. The oxidative metabolism of the PMNs was studied by measuring the chemiluminescence generated by virus-treated PMNs after incubation with zymosan. Chemotaxis was measured under agarose. After incubation with 107 EID50 units of influenza virus, PMNs ingested only 35 % of the bacteria, whereas control leukocytes ingested over 80 %. Influenza virus also reduced the mobility of the PMNs and markedly suppressed the generation of chemiluminiscence. UV-killed virus with intact neuraminidase produced similar effects but virus with heat-inactivated neuraminidase did not. Virus envelope-neuraminidase may be responsible for some of the effects of the virus on the PMNs.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Medical Microbiology</term></item><item><term>Internal Medicine</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1982-06-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-7W591876-B/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Berlin/Heidelberg</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>10096</JournalID><JournalPrintISSN>0722-2211</JournalPrintISSN><JournalElectronicISSN>1435-4373</JournalElectronicISSN><JournalTitle>European Journal of Clinical Microbiology</JournalTitle><JournalAbbreviatedTitle>Eur. 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Since the mechanisms by which the viruses affect neutrophil function are not well understood, we studied the function of polymorphonuclear leukocytes (PMNs) after incubation with influenza virus. Phagocytosis was assayed by incubating influenza virus (strain type A-Texas-77 [H<Subscript>2</Subscript>N<Subscript>2</Subscript>]) treated leukocytes with<Superscript>3</Superscript>H-thymidine-labelled staphylococci. The oxidative metabolism of the PMNs was studied by measuring the chemiluminescence generated by virus-treated PMNs after incubation with zymosan. Chemotaxis was measured under agarose. After incubation with 10<Superscript>7</Superscript> EID<Subscript>50</Subscript> units of influenza virus, PMNs ingested only 35 % of the bacteria, whereas control leukocytes ingested over 80 %. Influenza virus also reduced the mobility of the PMNs and markedly suppressed the generation of chemiluminiscence. UV-killed virus with intact neuraminidase produced similar effects but virus with heat-inactivated neuraminidase did not. Virus envelope-neuraminidase may be responsible for some of the effects of the virus on the PMNs.</Para></Abstract></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effect of influenza viras on phagocytic cells</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Effect of influenza viras on phagocytic cells</title></titleInfo><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Debets-Ossenkopp</namePart><affiliation>Microbiology Laboratory, State University Utrecht, Catharijnesingel 59, 3511, GG Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="given">L.</namePart><namePart type="family">Mills</namePart><affiliation>Microbiology Laboratory, State University Utrecht, Catharijnesingel 59, 3511, GG Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="given">C.</namePart><namePart type="family">van Dijk</namePart><affiliation>Microbiology Laboratory, State University Utrecht, Catharijnesingel 59, 3511, GG Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="given">A.</namePart><namePart type="family">Verbrugh</namePart><affiliation>Microbiology Laboratory, State University Utrecht, Catharijnesingel 59, 3511, GG Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">J.</namePart><namePart type="family">Verhoef</namePart><affiliation>Microbiology Laboratory, State University Utrecht, Catharijnesingel 59, 3511, GG Utrecht, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateIssued encoding="w3cdtf">1982-06-01</dateIssued><copyrightDate encoding="w3cdtf">1982</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Many viral infections predispose to bacterial superinfection, and it has been suggested that the increased susceptibility to bacterial infections is at least in part due to the effect of virus on the phagocytic cell function. Since the mechanisms by which the viruses affect neutrophil function are not well understood, we studied the function of polymorphonuclear leukocytes (PMNs) after incubation with influenza virus. Phagocytosis was assayed by incubating influenza virus (strain type A-Texas-77 [H2N2]) treated leukocytes with3H-thymidine-labelled staphylococci. The oxidative metabolism of the PMNs was studied by measuring the chemiluminescence generated by virus-treated PMNs after incubation with zymosan. Chemotaxis was measured under agarose. After incubation with 107 EID50 units of influenza virus, PMNs ingested only 35 % of the bacteria, whereas control leukocytes ingested over 80 %. Influenza virus also reduced the mobility of the PMNs and markedly suppressed the generation of chemiluminiscence. UV-killed virus with intact neuraminidase produced similar effects but virus with heat-inactivated neuraminidase did not. Virus envelope-neuraminidase may be responsible for some of the effects of the virus on the PMNs.</abstract><note>Original Articles</note><relatedItem type="host"><titleInfo><title>European Journal of Clinical Microbiology</title></titleInfo><titleInfo type="abbreviated"><title>Eur. J, Clin. Microbiol.</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">1982-06-01</dateIssued><copyrightDate encoding="w3cdtf">1982</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Medical Microbiology</topic><topic>Internal Medicine</topic></subject><identifier type="ISSN">0722-2211</identifier><identifier type="eISSN">1435-4373</identifier><identifier type="JournalID">10096</identifier><identifier type="IssueArticleCount">15</identifier><identifier type="VolumeIssueCount">6</identifier><part><date>1982</date><detail type="volume"><number>1</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="pages"><start>171</start><end>177</end></extent></part><recordInfo><recordOrigin>Vieweg Publishing, 1982</recordOrigin></recordInfo></relatedItem><identifier type="istex">09BC710D957C6B17EB7C06F54AF9D98180C0B69F</identifier><identifier type="ark">ark:/67375/1BB-7W591876-B</identifier><identifier type="DOI">10.1007/BF02019619</identifier><identifier type="ArticleID">BF02019619</identifier><identifier type="ArticleID">Art10</identifier><accessCondition type="use and reproduction" contentType="copyright">Vieweg Publishing, 1982</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Vieweg Publishing, 1982</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-7W591876-B/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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