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[Production of early cytokines after infection with A/Leningrad/134/57 (H2N2) wide-type virus and cold-adapted attenuated vaccine viruses].

Identifieur interne : 002D95 ( Main/Exploration ); précédent : 002D94; suivant : 002D96

[Production of early cytokines after infection with A/Leningrad/134/57 (H2N2) wide-type virus and cold-adapted attenuated vaccine viruses].

Auteurs : A R Rekstin ; K. Lu ; D. Kats ; L G Rudenko

Source :

RBID : pubmed:16756175

Descripteurs français

English descriptors

Abstract

The production of proinflammatory cytokines was studied following experimental infection of BALB/c mice with influenza viruses that differed in virulence. The generation of TNF-alpha, IL-6, IL-12, and IFN-gamma was investigated in the lung homogenates in the early periods after intranasal infection of mice with A/Leningrad/134/57 (H2N2) wild-type virus and cold-adapted attenuated vaccine viruses: A/Leningrad/134/17157 (H2N2) and A/Leningrad/134/47/57 (H2N2). Wild-type virus induced substantially higher levels of proinflammatory cytokines: TNF-alpha, IL-6, IL-12, and IFN-gamma. After infection with the cold-adapted viruses, the levels of the cytokines were reduced as compared to those induced by the wild-type virus. The A/Leningrad/134/47/57 virus was marked by a noticeable production of IL-6 and IFN-gamma in the murine lung, but it was less than with wild-type virus infection. At the same time, the more attenuated strain A/Leningrad/134/47/57 induced TNF-alpha and IFN-gamma in the quantities similar to those in the control animals. Thus, a response of proinflammatory cytokines in early infection in the murine lung depended on the level of viral replication in the lower respiratory tract and on the attenuation of influenza virus strains.

PubMed: 16756175


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Le document en format XML

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<term>Female</term>
<term>Influenza A Virus, H2N2 Subtype (immunology)</term>
<term>Influenza Vaccines (administration & dosage)</term>
<term>Influenza Vaccines (immunology)</term>
<term>Interferon-gamma (biosynthesis)</term>
<term>Interleukin-12 (biosynthesis)</term>
<term>Interleukin-6 (biosynthesis)</term>
<term>Lung (immunology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Orthomyxoviridae Infections (immunology)</term>
<term>Time Factors</term>
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<term>Administration par voie nasale</term>
<term>Animaux</term>
<term>Basse température</term>
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<term>Facteur de nécrose tumorale alpha (biosynthèse)</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Infections à Orthomyxoviridae (immunologie)</term>
<term>Interféron gamma (biosynthèse)</term>
<term>Interleukine-12 (biosynthèse)</term>
<term>Interleukine-6 (biosynthèse)</term>
<term>Poumon (immunologie)</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Sous-type H2N2 du virus de la grippe A (immunologie)</term>
<term>Vaccins antigrippaux (administration et posologie)</term>
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<div type="abstract" xml:lang="en">The production of proinflammatory cytokines was studied following experimental infection of BALB/c mice with influenza viruses that differed in virulence. The generation of TNF-alpha, IL-6, IL-12, and IFN-gamma was investigated in the lung homogenates in the early periods after intranasal infection of mice with A/Leningrad/134/57 (H2N2) wild-type virus and cold-adapted attenuated vaccine viruses: A/Leningrad/134/17157 (H2N2) and A/Leningrad/134/47/57 (H2N2). Wild-type virus induced substantially higher levels of proinflammatory cytokines: TNF-alpha, IL-6, IL-12, and IFN-gamma. After infection with the cold-adapted viruses, the levels of the cytokines were reduced as compared to those induced by the wild-type virus. The A/Leningrad/134/47/57 virus was marked by a noticeable production of IL-6 and IFN-gamma in the murine lung, but it was less than with wild-type virus infection. At the same time, the more attenuated strain A/Leningrad/134/47/57 induced TNF-alpha and IFN-gamma in the quantities similar to those in the control animals. Thus, a response of proinflammatory cytokines in early infection in the murine lung depended on the level of viral replication in the lower respiratory tract and on the attenuation of influenza virus strains.</div>
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