Effect of influenza virus on phagocytic cells.
Identifieur interne : 000560 ( PubMed/Curation ); précédent : 000559; suivant : 000561Effect of influenza virus 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.
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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 with 3H-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(7) 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.
DOI: 10.1007/bf02019619
PubMed: 7173182
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Verhoef</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1982">1982</date><idno type="RBID">pubmed:7173182</idno><idno type="pmid">7173182</idno><idno type="doi">10.1007/bf02019619</idno><idno type="wicri:Area/PubMed/Corpus">000560</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000560</idno><idno type="wicri:Area/PubMed/Curation">000560</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000560</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effect of influenza virus on phagocytic cells.</title><author><name sortKey="Debets Ossenkopp, Y" sort="Debets Ossenkopp, Y" uniqKey="Debets Ossenkopp Y" first="Y" last="Debets-Ossenkopp">Y. Debets-Ossenkopp</name></author><author><name sortKey="Mills, E L" sort="Mills, E L" uniqKey="Mills E" first="E L" last="Mills">E L Mills</name></author><author><name sortKey="Van Dijk, W C" sort="Van Dijk, W C" uniqKey="Van Dijk W" first="W C" last="Van Dijk">W C Van Dijk</name></author><author><name sortKey="Verbrugh, H A" sort="Verbrugh, H A" uniqKey="Verbrugh H" first="H A" last="Verbrugh">H A Verbrugh</name></author><author><name sortKey="Verhoef, J" sort="Verhoef, J" uniqKey="Verhoef J" first="J" last="Verhoef">J. Verhoef</name></author></analytic><series><title level="j">European journal of clinical microbiology</title><idno type="ISSN">0722-2211</idno><imprint><date when="1982" type="published">1982</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Blood Bactericidal Activity</term><term>Cell Survival</term><term>Chemotaxis, Leukocyte</term><term>Humans</term><term>Influenza A virus (immunology)</term><term>Luminescent Measurements</term><term>Neutrophils (immunology)</term><term>Phagocytes (immunology)</term><term>Phagocytosis</term><term>Virus Replication</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activité bactéricide du sang</term><term>Chimiotaxie des leucocytes</term><term>Granulocytes neutrophiles (immunologie)</term><term>Humains</term><term>Mesures de luminescence</term><term>Phagocytes (immunologie)</term><term>Phagocytose</term><term>Réplication virale</term><term>Survie cellulaire</term><term>Virus de la grippe A (immunologie)</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Granulocytes neutrophiles</term><term>Phagocytes</term><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A virus</term><term>Neutrophils</term><term>Phagocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Blood Bactericidal Activity</term><term>Cell Survival</term><term>Chemotaxis, Leukocyte</term><term>Humans</term><term>Luminescent Measurements</term><term>Phagocytosis</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activité bactéricide du sang</term><term>Chimiotaxie des leucocytes</term><term>Humains</term><term>Mesures de luminescence</term><term>Phagocytose</term><term>Réplication virale</term><term>Survie cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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 with 3H-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(7) 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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">7173182</PMID><DateCompleted><Year>1983</Year><Month>02</Month><Day>14</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>04</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0722-2211</ISSN><JournalIssue CitedMedium="Print"><Volume>1</Volume><Issue>3</Issue><PubDate><Year>1982</Year><Month>Jun</Month></PubDate></JournalIssue><Title>European journal of clinical microbiology</Title><ISOAbbreviation>Eur. J. Clin. Microbiol.</ISOAbbreviation></Journal><ArticleTitle>Effect of influenza virus on phagocytic cells.</ArticleTitle><Pagination><MedlinePgn>171-7</MedlinePgn></Pagination><Abstract><AbstractText>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 with 3H-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(7) 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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Debets-Ossenkopp</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Mills</LastName><ForeName>E L</ForeName><Initials>EL</Initials></Author><Author ValidYN="Y"><LastName>van Dijk</LastName><ForeName>W C</ForeName><Initials>WC</Initials></Author><Author ValidYN="Y"><LastName>Verbrugh</LastName><ForeName>H A</ForeName><Initials>HA</Initials></Author><Author ValidYN="Y"><LastName>Verhoef</LastName><ForeName>J</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Eur J Clin 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