Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by Coronavirus-19 (COVI-19 or SARS-CoV-2): anti-inflammatory strategies.
Identifieur interne : 000655 ( Main/Exploration ); précédent : 000654; suivant : 000656Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by Coronavirus-19 (COVI-19 or SARS-CoV-2): anti-inflammatory strategies.
Auteurs : P. Conti [Italie] ; G. Ronconi [Italie] ; A. Caraffa [Italie] ; C. Gallenga [Italie] ; R. Ross [États-Unis] ; I. Frydas [Grèce] ; S. Kritas [Grèce]Source :
- Journal of biological regulators and homeostatic agents [ 0393-974X ] ; 2020.
Abstract
Coronavirus-19 (COVI-19) involves humans as well as animals and may cause serious damage to the respiratory tract, including the lung: coronavirus disease (COVID-19). This pathogenic virus has been identified in swabs performed on the throat and nose of patients who suffer from or are suspected of the disease. When COVI-19 infect the upper and lower respiratory tract it can cause mild or highly acute respiratory syndrome with consequent release of pro-inflammatory cytokines, including interleukin (IL)-1β and IL-6.
The binding of COVI-19 to the Toll Like Receptor (TLR) causes the release of pro-IL-1β which is cleaved by caspase-1, followed by inflammasome activation and production of active mature IL-1β which is a mediator of lung inflammation, fever and fibrosis. Suppression of pro-inflammatory IL-1 family members and IL-6 have been shown to have a therapeutic effect in many inflammatory diseases, including viral infections.
Cytokine IL-37 has the ability to suppress innate and acquired immune response and also has the capacity to inhibit inflammation by acting on IL-18Rα receptor. IL-37 performs its immunosuppressive activity by acting on mTOR and increasing the adenosine monophosphate (AMP) kinase. This cytokine inhibits class II histocompatibility complex (MHC) molecules and inflammation in inflammatory diseases by suppressing MyD88 and subsequently IL-1β, IL-6, TNF and CCL2. The suppression of IL-1β by IL-37 in inflammatory state induced by coronavirus-19 can have a new therapeutic effect previously unknown. Another inhibitory cytokine is IL-38, the newest cytokine of the IL-1 family members, produced by several immune cells including B cells and macrophages.
IL-38 is also a suppressor cytokine which inhibits IL-1β and other pro-inflammatory IL-family members. IL-38 is a potential therapeutic cytokine which inhibits inflammation in viral infections including that caused by coronavirus-19, providing a new relevant strategy.
DOI: 10.23812/CONTI-E
PubMed: 32171193
Affiliations:
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Conti</name><affiliation wicri:level="1"><nlm:affiliation>Postgraduate Medical School, University of Chieti, Chieti, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Postgraduate Medical School, University of Chieti, Chieti</wicri:regionArea><wicri:noRegion>Chieti</wicri:noRegion></affiliation></author><author><name sortKey="Ronconi, G" sort="Ronconi, G" uniqKey="Ronconi G" first="G" last="Ronconi">G. Ronconi</name><affiliation wicri:level="3"><nlm:affiliation>Clinica dei Pazienti del Territorio, Fondazione Policlinico Gemelli, Rome, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Clinica dei Pazienti del Territorio, Fondazione Policlinico Gemelli, Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Caraffa, A" sort="Caraffa, A" uniqKey="Caraffa A" first="A" last="Caraffa">A. Caraffa</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy, University of Camerino, Camerino, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>School of Pharmacy, University of Camerino, Camerino</wicri:regionArea><wicri:noRegion>Camerino</wicri:noRegion></affiliation></author><author><name sortKey="Gallenga, C" sort="Gallenga, C" uniqKey="Gallenga C" first="C" last="Gallenga">C. Gallenga</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Sciences and Specialist Surgery, Section of Ophthalmology, University of Ferrara, Ferrara, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Biomedical Sciences and Specialist Surgery, Section of Ophthalmology, University of Ferrara, Ferrara</wicri:regionArea><wicri:noRegion>Ferrara</wicri:noRegion></affiliation></author><author><name sortKey="Ross, R" sort="Ross, R" uniqKey="Ross R" first="R" last="Ross">R. Ross</name><affiliation wicri:level="2"><nlm:affiliation>University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA</wicri:regionArea><placeName><region type="state">Pennsylvanie</region></placeName></affiliation></author><author><name sortKey="Frydas, I" sort="Frydas, I" uniqKey="Frydas I" first="I" last="Frydas">I. Frydas</name><affiliation wicri:level="1"><nlm:affiliation>Aristotelian University, Thessaloniki, Greece.</nlm:affiliation><country xml:lang="fr">Grèce</country><wicri:regionArea>Aristotelian University, Thessaloniki</wicri:regionArea><wicri:noRegion>Thessaloniki</wicri:noRegion></affiliation></author><author><name sortKey="Kritas, S" sort="Kritas, S" uniqKey="Kritas S" first="S" last="Kritas">S. Kritas</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Infectious Diseases, School of Veterinary Medicine, Aristotle University of Thessaloniki, Macedonia, Greece.</nlm:affiliation><country xml:lang="fr">Grèce</country><wicri:regionArea>Department of Microbiology and Infectious Diseases, School of Veterinary Medicine, Aristotle University of Thessaloniki, Macedonia</wicri:regionArea><wicri:noRegion>Macedonia</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of biological regulators and homeostatic agents</title><idno type="ISSN">0393-974X</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Coronavirus-19 (COVI-19) involves humans as well as animals and may cause serious damage to the respiratory tract, including the lung: coronavirus disease (COVID-19). This pathogenic virus has been identified in swabs performed on the throat and nose of patients who suffer from or are suspected of the disease. When COVI-19 infect the upper and lower respiratory tract it can cause mild or highly acute respiratory syndrome with consequent release of pro-inflammatory cytokines, including interleukin (IL)-1β and IL-6.
The binding of COVI-19 to the Toll Like Receptor (TLR) causes the release of pro-IL-1β which is cleaved by caspase-1, followed by inflammasome activation and production of active mature IL-1β which is a mediator of lung inflammation, fever and fibrosis. Suppression of pro-inflammatory IL-1 family members and IL-6 have been shown to have a therapeutic effect in many inflammatory diseases, including viral infections.
Cytokine IL-37 has the ability to suppress innate and acquired immune response and also has the capacity to inhibit inflammation by acting on IL-18Rα receptor. IL-37 performs its immunosuppressive activity by acting on mTOR and increasing the adenosine monophosphate (AMP) kinase. This cytokine inhibits class II histocompatibility complex (MHC) molecules and inflammation in inflammatory diseases by suppressing MyD88 and subsequently IL-1β, IL-6, TNF and CCL2. The suppression of IL-1β by IL-37 in inflammatory state induced by coronavirus-19 can have a new therapeutic effect previously unknown. Another inhibitory cytokine is IL-38, the newest cytokine of the IL-1 family members, produced by several immune cells including B cells and macrophages.
IL-38 is also a suppressor cytokine which inhibits IL-1β and other pro-inflammatory IL-family members. IL-38 is a potential therapeutic cytokine which inhibits inflammation in viral infections including that caused by coronavirus-19, providing a new relevant strategy.</div></front></TEI><affiliations><list><country><li>Grèce</li><li>Italie</li><li>États-Unis</li></country><region><li>Latium</li><li>Pennsylvanie</li></region><settlement><li>Rome</li></settlement></list><tree><country name="Italie"><noRegion><name sortKey="Conti, P" sort="Conti, P" uniqKey="Conti P" first="P" last="Conti">P. Conti</name></noRegion><name sortKey="Caraffa, A" sort="Caraffa, A" uniqKey="Caraffa A" first="A" last="Caraffa">A. Caraffa</name><name sortKey="Gallenga, C" sort="Gallenga, C" uniqKey="Gallenga C" first="C" last="Gallenga">C. Gallenga</name><name sortKey="Ronconi, G" sort="Ronconi, G" uniqKey="Ronconi G" first="G" last="Ronconi">G. Ronconi</name></country><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Ross, R" sort="Ross, R" uniqKey="Ross R" first="R" last="Ross">R. Ross</name></region></country><country name="Grèce"><noRegion><name sortKey="Frydas, I" sort="Frydas, I" uniqKey="Frydas I" first="I" last="Frydas">I. Frydas</name></noRegion><name sortKey="Kritas, S" sort="Kritas, S" uniqKey="Kritas S" first="S" last="Kritas">S. Kritas</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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