The role of C5a in acute lung injury induced by highly pathogenic viral infections
Identifieur interne : 001216 ( Main/Exploration ); précédent : 001215; suivant : 001217The role of C5a in acute lung injury induced by highly pathogenic viral infections
Auteurs : Renxi Wang [République populaire de Chine] ; He Xiao [République populaire de Chine] ; Renfeng Guo [États-Unis, Allemagne] ; Yan Li [République populaire de Chine] ; Beifen Shen [République populaire de Chine]Source :
- Emerging Microbes & Infections [ 2222-1751 ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- immunologie : Lésion pulmonaire aigüe, Maladies virales.
- métabolisme : Complément C5a, Espèces réactives de l'oxygène.
- pathogénicité : Virus.
- virologie : Lésion pulmonaire aigüe.
- Animaux, Humains, Maladies virales, Modèles animaux de maladie humaine.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Complement C5a, Reactive Oxygen Species.
- complications : Virus Diseases.
- immunology : Acute Lung Injury, Virus Diseases.
- pathogenicity : Viruses.
- virology : Acute Lung Injury.
- Animals, Disease Models, Animal, Humans.
Abstract
The complement system, an important part of innate immunity, plays a critical role in pathogen clearance. Unregulated complement activation is likely to play a crucial role in the pathogenesis of acute lung injury (ALI) induced by highly pathogenic virus including influenza A viruses H5N1, H7N9, and severe acute respiratory syndrome (SARS) coronavirus. In highly pathogenic virus-induced acute lung diseases, high levels of chemotactic and anaphylatoxic C5a were produced as a result of excessive complement activaiton. Overproduced C5a displays powerful biological activities in activation of phagocytic cells, generation of oxidants, and inflammatory sequelae named “cytokine storm”, and so on. Blockade of C5a signaling have been implicated in the treatment of ALI induced by highly pathogenic virus. Herein, we review the literature that links C5a and ALI, and review our understanding of the mechanisms by which C5a affects ALI during highly pathogenic viral infection. In particular, we discuss the potential of the blockade of C5a signaling to treat ALI induced by highly pathogenic viruses.
Url:
DOI: 10.1038/emi.2015.28
PubMed: 26060601
PubMed Central: 4451266
Affiliations:
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Xiao</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Laboratory of Immunology, Institute of Basic Medical Sciences</institution>, Beijing 100850,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Guo, Renfeng" sort="Guo, Renfeng" uniqKey="Guo R" first="Renfeng" last="Guo">Renfeng Guo</name><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Pathology, University of Michigan</institution>, Ann Arbor, Michigan 48109,<country>USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>InflaRx GmbH</institution>, Jena 07745,<country>Germany</country></nlm:aff><country xml:lang="fr">Allemagne</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Li, Yan" sort="Li, Yan" uniqKey="Li Y" first="Yan" last="Li">Yan Li</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Laboratory of Immunology, Institute of Basic Medical Sciences</institution>, Beijing 100850,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Shen, Beifen" sort="Shen, Beifen" uniqKey="Shen B" first="Beifen" last="Shen">Beifen Shen</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Laboratory of Immunology, Institute of Basic Medical Sciences</institution>, Beijing 100850,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Emerging Microbes & Infections</title><idno type="eISSN">2222-1751</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Lung Injury (immunology)</term><term>Acute Lung Injury (virology)</term><term>Animals</term><term>Complement C5a (metabolism)</term><term>Disease Models, Animal</term><term>Humans</term><term>Reactive Oxygen Species (metabolism)</term><term>Virus Diseases (complications)</term><term>Virus Diseases (immunology)</term><term>Viruses (pathogenicity)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Complément C5a (métabolisme)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Humains</term><term>Lésion pulmonaire aigüe (immunologie)</term><term>Lésion pulmonaire aigüe (virologie)</term><term>Maladies virales ()</term><term>Maladies virales (immunologie)</term><term>Modèles animaux de maladie humaine</term><term>Virus (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Complement C5a</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Virus Diseases</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lésion pulmonaire aigüe</term><term>Maladies virales</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Acute Lung Injury</term><term>Virus Diseases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Complément C5a</term><term>Espèces réactives de l'oxygène</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Viruses</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Lésion pulmonaire aigüe</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Acute Lung Injury</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Maladies virales</term><term>Modèles animaux de maladie humaine</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The complement system, an important part of innate immunity, plays a critical role in pathogen clearance. Unregulated complement activation is likely to play a crucial role in the pathogenesis of acute lung injury (ALI) induced by highly pathogenic virus including influenza A viruses H5N1, H7N9, and severe acute respiratory syndrome (SARS) coronavirus. In highly pathogenic virus-induced acute lung diseases, high levels of chemotactic and anaphylatoxic C5a were produced as a result of excessive complement activaiton. Overproduced C5a displays powerful biological activities in activation of phagocytic cells, generation of oxidants, and inflammatory sequelae named “cytokine storm”, and so on. Blockade of C5a signaling have been implicated in the treatment of ALI induced by highly pathogenic virus. Herein, we review the literature that links C5a and ALI, and review our understanding of the mechanisms by which C5a affects ALI during highly pathogenic viral infection. In particular, we discuss the potential of the blockade of C5a signaling to treat ALI induced by highly pathogenic viruses.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Ackerman, Sk" uniqKey="Ackerman S">SK Ackerman</name></author><author><name sortKey="Friend, Ps" uniqKey="Friend P">PS Friend</name></author><author><name sortKey="Hoidal, Jr" uniqKey="Hoidal J">JR Hoidal</name></author><author><name sortKey="Douglas, Sd" uniqKey="Douglas S">SD Douglas</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cole, Fs" uniqKey="Cole F">FS Cole</name></author><author><name sortKey="Matthews, Wj" uniqKey="Matthews W">WJ Matthews</name></author><author><name sortKey="Rossing, Th" uniqKey="Rossing T">TH Rossing</name></author><author><name sortKey="Gash, Dj" uniqKey="Gash D">DJ Gash</name></author><author><name sortKey="Lichtenberg, Na" uniqKey="Lichtenberg N">NA Lichtenberg</name></author><author><name 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Sun</name></author><author><name sortKey="Guo, Rf" uniqKey="Guo R">RF Guo</name></author><author><name sortKey="Gao, H" uniqKey="Gao H">H Gao</name></author><author><name sortKey="Sarma, Jv" uniqKey="Sarma J">JV Sarma</name></author><author><name sortKey="Zetoune, Fs" uniqKey="Zetoune F">FS Zetoune</name></author><author><name sortKey="Ward, Pa" uniqKey="Ward P">PA Ward</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Proctor, Lm" uniqKey="Proctor L">LM Proctor</name></author><author><name sortKey="Strachan, Aj" uniqKey="Strachan A">AJ Strachan</name></author><author><name sortKey="Woodruff, Tm" uniqKey="Woodruff T">TM Woodruff</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bosmann, M" uniqKey="Bosmann M">M Bosmann</name></author><author><name sortKey="Ward, Pa" uniqKey="Ward P">PA Ward</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bhatia, M" uniqKey="Bhatia M">M Bhatia</name></author><author><name sortKey="Moochhala, S" uniqKey="Moochhala S">S Moochhala</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Osterholm, Mt" uniqKey="Osterholm M">MT Osterholm</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Haque, A" uniqKey="Haque A">A Haque</name></author><author><name sortKey="Hober, D" uniqKey="Hober D">D Hober</name></author><author><name sortKey="Kasper, Lh" uniqKey="Kasper L">LH Kasper</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Barnes, Pj" uniqKey="Barnes P">PJ Barnes</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ansari, Aa" uniqKey="Ansari A">AA Ansari</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Allemagne</li><li>République populaire de Chine</li><li>États-Unis</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Wang, Renxi" sort="Wang, Renxi" uniqKey="Wang R" first="Renxi" last="Wang">Renxi Wang</name></noRegion><name sortKey="Li, Yan" sort="Li, Yan" uniqKey="Li Y" first="Yan" last="Li">Yan Li</name><name sortKey="Shen, Beifen" sort="Shen, Beifen" uniqKey="Shen B" first="Beifen" last="Shen">Beifen Shen</name><name sortKey="Xiao, He" sort="Xiao, He" uniqKey="Xiao H" first="He" last="Xiao">He Xiao</name></country><country name="États-Unis"><noRegion><name sortKey="Guo, Renfeng" sort="Guo, Renfeng" uniqKey="Guo R" first="Renfeng" last="Guo">Renfeng Guo</name></noRegion></country><country name="Allemagne"><noRegion><name sortKey="Guo, Renfeng" sort="Guo, Renfeng" uniqKey="Guo R" first="Renfeng" last="Guo">Renfeng Guo</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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