StressCovidV1, PubMed, Checkpoint, bibRecord, 000645

Chronic heat stress weakened the innate immunity and increased the virulence of highly pathogenic avian influenza virus H5N1 in mice.

Identifieur interne : 000645 ( PubMed/Checkpoint ); précédent : 000644; suivant : 000646

Chronic 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 Wang

Source :

Journal of biomedicine & biotechnology [ 1110-7251 ] ; 2011.

RBID : pubmed:21687549

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:

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 000627
to stream PubMed, to step Curation: 000625

Links to Exploration step

pubmed:21687549

Le document en format XML

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<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>
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<Abstract><AbstractText>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.</AbstractText>
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Chronic heat stress weakened the innate immunity and increased the virulence of highly pathogenic avian influenza virus H5N1 in mice.

Chronic heat stress weakened the innate immunity and increased the virulence of highly pathogenic avian influenza virus H5N1 in mice.

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