Chronic heat stress weakened the innate immunity and increased the virulence of highly pathogenic avian influenza virus H5N1 in mice.
Identifieur interne : 001559 ( Main/Exploration ); précédent : 001558; suivant : 001560Chronic heat stress weakened the innate immunity and increased the virulence of highly pathogenic avian influenza virus H5N1 in mice.
Auteurs : Yi Jin [République populaire de Chine] ; Yanxin Hu ; Deping Han ; Ming WangSource :
- Journal of biomedicine & biotechnology [ 1110-7251 ] ; 2011.
Descripteurs français
- KwdFr :
- Animaux, Appareil respiratoire (immunologie), Appareil respiratoire (virologie), Cellules dendritiques (immunologie), Chiens, Femelle, Immunité innée, Infections à Orthomyxoviridae (immunologie), Infections à Orthomyxoviridae (virologie), Interactions hôte-pathogène (immunologie), Interféron bêta (métabolisme), Interleukine-6 (métabolisme), Lignée cellulaire, Maladie chronique, Rein (cytologie), Réaction de choc thermique (immunologie), Souris, Souris de lignée BALB C, Sous-type H5N1 du virus de la grippe A (pathogénicité), Troubles dus à la chaleur (immunologie), Virulence, Virus de la grippe A (pathogénicité).
- MESH :
- cytologie : Rein.
- immunologie : Appareil respiratoire, Cellules dendritiques, Infections à Orthomyxoviridae, Interactions hôte-pathogène, Réaction de choc thermique, Troubles dus à la chaleur.
- métabolisme : Interféron bêta, Interleukine-6.
- pathogénicité : Sous-type H5N1 du virus de la grippe A, Virus de la grippe A.
- virologie : Appareil respiratoire, Infections à Orthomyxoviridae.
- Animaux, Chiens, Femelle, Immunité innée, Lignée cellulaire, Maladie chronique, Souris, Souris de lignée BALB C, Virulence.
English descriptors
- KwdEn :
- Animals, Cell Line, Chronic Disease, Dendritic Cells (immunology), Dogs, Female, Heat Stress Disorders (immunology), Heat-Shock Response (immunology), Host-Pathogen Interactions (immunology), Immunity, Innate, Influenza A Virus, H5N1 Subtype (pathogenicity), Influenza A virus (pathogenicity), Interferon-beta (metabolism), Interleukin-6 (metabolism), Kidney (cytology), Mice, Mice, Inbred BALB C, Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (virology), Respiratory System (immunology), Respiratory System (virology), Virulence.
- MESH :
- chemical , metabolism : Interferon-beta, Interleukin-6.
- cytology : Kidney.
- immunology : Dendritic Cells, Heat Stress Disorders, Heat-Shock Response, Host-Pathogen Interactions, Orthomyxoviridae Infections, Respiratory System.
- pathogenicity : Influenza A Virus, H5N1 Subtype, Influenza A virus.
- virology : Orthomyxoviridae Infections, Respiratory System.
- Animals, Cell Line, Chronic Disease, Dogs, Female, Immunity, Innate, Mice, Mice, Inbred BALB C, Virulence.
Abstract
Chronic heat stress (CHS) can negatively affect immune response in animals. In this study we assessed the effects of CHS on host innate immunity and avian influenza virus H5N1 infection in mice. Mice were divided into two groups: CHS and thermally neutral (TN). The CHS treatment group exhibited reduced local immunity in the respiratory tract, including the number of pulmonary alveolar macrophages and lesions in the nasal mucosa, trachea, and lungs. Meanwhile, CHS retarded dendritic cells (DCs) maturation and reduced the mRNA levels of IL-6 and IFN-β significantly (P < .05). After the CHS treatment, mice were infected with H5N1 virus. The mortality rate and viral load in the lungs of CHS group were higher than those of TN group. The results suggest that the CHS treatment could suppress local immunity in the respiratory tract and innate host immunity in mice significantly and moderately increased the virulence in H5N1-infected mice.
DOI: 10.1155/2011/367846
PubMed: 21687549
Affiliations:
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Yanxin" sort="Hu, Yanxin" uniqKey="Hu Y" first="Yanxin" last="Hu">Yanxin Hu</name></author><author><name sortKey="Han, Deping" sort="Han, Deping" uniqKey="Han D" first="Deping" last="Han">Deping Han</name></author><author><name sortKey="Wang, Ming" sort="Wang, Ming" uniqKey="Wang M" first="Ming" last="Wang">Ming Wang</name></author></analytic><series><title level="j">Journal of biomedicine & biotechnology</title><idno type="eISSN">1110-7251</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Chronic Disease</term><term>Dendritic Cells (immunology)</term><term>Dogs</term><term>Female</term><term>Heat Stress Disorders (immunology)</term><term>Heat-Shock Response (immunology)</term><term>Host-Pathogen Interactions (immunology)</term><term>Immunity, Innate</term><term>Influenza A Virus, H5N1 Subtype 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System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Chronic Disease</term><term>Dogs</term><term>Female</term><term>Immunity, Innate</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Virulence</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Chiens</term><term>Femelle</term><term>Immunité innée</term><term>Lignée cellulaire</term><term>Maladie chronique</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Virulence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Chronic heat stress (CHS) can negatively affect immune response in animals. In this study we assessed the effects of CHS on host innate immunity and avian influenza virus H5N1 infection in mice. Mice were divided into two groups: CHS and thermally neutral (TN). The CHS treatment group exhibited reduced local immunity in the respiratory tract, including the number of pulmonary alveolar macrophages and lesions in the nasal mucosa, trachea, and lungs. Meanwhile, CHS retarded dendritic cells (DCs) maturation and reduced the mRNA levels of IL-6 and IFN-β significantly (P < .05). After the CHS treatment, mice were infected with H5N1 virus. The mortality rate and viral load in the lungs of CHS group were higher than those of TN group. The results suggest that the CHS treatment could suppress local immunity in the respiratory tract and innate host immunity in mice significantly and moderately increased the virulence in H5N1-infected mice.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><noCountry><name sortKey="Han, Deping" sort="Han, Deping" uniqKey="Han D" first="Deping" last="Han">Deping Han</name><name sortKey="Hu, Yanxin" sort="Hu, Yanxin" uniqKey="Hu Y" first="Yanxin" last="Hu">Yanxin Hu</name><name sortKey="Wang, Ming" sort="Wang, Ming" uniqKey="Wang M" first="Ming" last="Wang">Ming Wang</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Jin, Yi" sort="Jin, Yi" uniqKey="Jin Y" first="Yi" last="Jin">Yi Jin</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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