Proinflammatory effects of the hemagglutinin protein of the avian influenza A (H7N9) virus and microRNA‑mediated homeostasis response in THP‑1 cells.
Identifieur interne : 000D11 ( Main/Exploration ); précédent : 000D10; suivant : 000D12Proinflammatory effects of the hemagglutinin protein of the avian influenza A (H7N9) virus and microRNA‑mediated homeostasis response in THP‑1 cells.
Auteurs : Shaobo Zhang [République populaire de Chine] ; Dayong Gu [République populaire de Chine] ; Xiaoxi Ouyang [République populaire de Chine] ; Weidong Xie [République populaire de Chine]Source :
- Molecular medicine reports [ 1791-3004 ] ; 2015.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Glycoprotéine hémagglutinine du virus influenza (métabolisme), Homéostasie, Humains, Interleukine-1 alpha (immunologie), Interleukine-1 bêta (immunologie), Interleukine-6 (immunologie), Lignée cellulaire tumorale, Protéines virales (métabolisme), Récepteur de type Toll-4 (métabolisme), Régulation de l'expression des gènes, Sous-type H7N9 du virus de la grippe A, Stress physiologique, Techniques de knock-down de gènes, microARN (génétique), microARN (métabolisme).
- MESH :
- génétique : ARN messager, microARN.
- immunologie : Interleukine-1 alpha, Interleukine-1 bêta, Interleukine-6.
- métabolisme : ARN messager, Glycoprotéine hémagglutinine du virus influenza, Protéines virales, Récepteur de type Toll-4, microARN.
- Homéostasie, Humains, Lignée cellulaire tumorale, Régulation de l'expression des gènes, Sous-type H7N9 du virus de la grippe A, Stress physiologique, Techniques de knock-down de gènes.
English descriptors
- KwdEn :
- Cell Line, Tumor, Gene Expression Regulation, Gene Knockdown Techniques, Hemagglutinin Glycoproteins, Influenza Virus (metabolism), Homeostasis, Humans, Influenza A Virus, H7N9 Subtype, Interleukin-1alpha (immunology), Interleukin-1beta (immunology), Interleukin-6 (immunology), MicroRNAs (genetics), MicroRNAs (metabolism), RNA, Messenger (genetics), RNA, Messenger (metabolism), Stress, Physiological, Toll-Like Receptor 4 (metabolism), Viral Proteins (metabolism).
- MESH :
- chemical , genetics : MicroRNAs, RNA, Messenger.
- chemical , immunology : Interleukin-1alpha, Interleukin-1beta, Interleukin-6.
- chemical , metabolism : Hemagglutinin Glycoproteins, Influenza Virus, MicroRNAs, RNA, Messenger, Toll-Like Receptor 4, Viral Proteins.
- Cell Line, Tumor, Gene Expression Regulation, Gene Knockdown Techniques, Homeostasis, Humans, Influenza A Virus, H7N9 Subtype, Stress, Physiological.
Abstract
The pathology and immunological responses to hemagglutinin (HA) from H7N9 avian influenza viruses in humans remain unclear. The present study aimed to investigate the proinflammatory activity of the HA protein obtained from H7N9 viruses and the mechanisms underlying the homeostasis of microRNAs (miRNAs) in response to inflammatory stimuli. The expression of proinflammatory factors and miRNAs was assayed in the THP‑1 cells using reverse transcription‑quantitative polymerase chain reaction. Results showed that HA significantly increased the expression of interleukin (IL)‑1α, IL‑1β and IL‑6 in the THP‑1 cells. Furthermore, HA and lipopolysaccharide exhibited synergic effects on the expression of IL‑1α, IL‑1β and IL‑6 in the THP‑1 cells. Let‑7e can target IL‑6 and inhibit its expression. Notably, HA significantly increased let‑7e expression in THP‑1 cells and decreased the let‑7e levels in the medium. However, the knockdown of toll‑like receptor 4 (TLR4) significantly attenuated the effects of HA. These results indicate that the HA can induce inflammatory stress and may trigger an miRNA‑mediated homeostasis response to this stress. The effects of HA appeared to be mediated by the TLR4 pathway.
DOI: 10.3892/mmr.2015.4142
PubMed: 26238163
Affiliations:
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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Shenzhen Key Lab of Health Science and Technology, Division of Life Science & Health, Graduate School at Shenzhen, Tsinghua University, Shenzhen, Guangdong 518055</wicri:regionArea><wicri:noRegion>Guangdong 518055</wicri:noRegion></affiliation></author></analytic><series><title level="j">Molecular medicine reports</title><idno type="eISSN">1791-3004</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Line, Tumor</term><term>Gene Expression Regulation</term><term>Gene Knockdown Techniques</term><term>Hemagglutinin Glycoproteins, Influenza Virus (metabolism)</term><term>Homeostasis</term><term>Humans</term><term>Influenza A Virus, H7N9 Subtype</term><term>Interleukin-1alpha (immunology)</term><term>Interleukin-1beta (immunology)</term><term>Interleukin-6 (immunology)</term><term>MicroRNAs (genetics)</term><term>MicroRNAs (metabolism)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Stress, Physiological</term><term>Toll-Like Receptor 4 (metabolism)</term><term>Viral Proteins (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Glycoprotéine hémagglutinine du virus influenza (métabolisme)</term><term>Homéostasie</term><term>Humains</term><term>Interleukine-1 alpha (immunologie)</term><term>Interleukine-1 bêta (immunologie)</term><term>Interleukine-6 (immunologie)</term><term>Lignée cellulaire tumorale</term><term>Protéines virales (métabolisme)</term><term>Récepteur de type Toll-4 (métabolisme)</term><term>Régulation de l'expression des gènes</term><term>Sous-type H7N9 du virus de la grippe A</term><term>Stress physiologique</term><term>Techniques de knock-down de gènes</term><term>microARN (génétique)</term><term>microARN (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>MicroRNAs</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Interleukin-1alpha</term><term>Interleukin-1beta</term><term>Interleukin-6</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hemagglutinin Glycoproteins, Influenza Virus</term><term>MicroRNAs</term><term>RNA, Messenger</term><term>Toll-Like Receptor 4</term><term>Viral Proteins</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>microARN</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Interleukine-1 alpha</term><term>Interleukine-1 bêta</term><term>Interleukine-6</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Glycoprotéine hémagglutinine du virus influenza</term><term>Protéines virales</term><term>Récepteur de type Toll-4</term><term>microARN</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line, Tumor</term><term>Gene Expression Regulation</term><term>Gene Knockdown Techniques</term><term>Homeostasis</term><term>Humans</term><term>Influenza A Virus, H7N9 Subtype</term><term>Stress, Physiological</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Homéostasie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Régulation de l'expression des gènes</term><term>Sous-type H7N9 du virus de la grippe A</term><term>Stress physiologique</term><term>Techniques de knock-down de gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pathology and immunological responses to hemagglutinin (HA) from H7N9 avian influenza viruses in humans remain unclear. The present study aimed to investigate the proinflammatory activity of the HA protein obtained from H7N9 viruses and the mechanisms underlying the homeostasis of microRNAs (miRNAs) in response to inflammatory stimuli. The expression of proinflammatory factors and miRNAs was assayed in the THP‑1 cells using reverse transcription‑quantitative polymerase chain reaction. Results showed that HA significantly increased the expression of interleukin (IL)‑1α, IL‑1β and IL‑6 in the THP‑1 cells. Furthermore, HA and lipopolysaccharide exhibited synergic effects on the expression of IL‑1α, IL‑1β and IL‑6 in the THP‑1 cells. Let‑7e can target IL‑6 and inhibit its expression. Notably, HA significantly increased let‑7e expression in THP‑1 cells and decreased the let‑7e levels in the medium. However, the knockdown of toll‑like receptor 4 (TLR4) significantly attenuated the effects of HA. These results indicate that the HA can induce inflammatory stress and may trigger an miRNA‑mediated homeostasis response to this stress. The effects of HA appeared to be mediated by the TLR4 pathway.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Shaobo" sort="Zhang, Shaobo" uniqKey="Zhang S" first="Shaobo" last="Zhang">Shaobo Zhang</name></noRegion><name sortKey="Gu, Dayong" sort="Gu, Dayong" uniqKey="Gu D" first="Dayong" last="Gu">Dayong Gu</name><name sortKey="Ouyang, Xiaoxi" sort="Ouyang, Xiaoxi" uniqKey="Ouyang X" first="Xiaoxi" last="Ouyang">Xiaoxi Ouyang</name><name sortKey="Xie, Weidong" sort="Xie, Weidong" uniqKey="Xie W" first="Weidong" last="Xie">Weidong Xie</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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