PMC:7102583 / 13133-15413 JSON TXT

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LitCovid-PubTator

LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T30","span":{"begin":739,"end":744},"obj":"Body_part"},{"id":"T31","span":{"begin":796,"end":809},"obj":"Body_part"},{"id":"T32","span":{"begin":976,"end":987},"obj":"Body_part"},{"id":"T33","span":{"begin":1302,"end":1306},"obj":"Body_part"},{"id":"T34","span":{"begin":1520,"end":1524},"obj":"Body_part"},{"id":"T35","span":{"begin":1837,"end":1841},"obj":"Body_part"},{"id":"T36","span":{"begin":2034,"end":2038},"obj":"Body_part"},{"id":"T37","span":{"begin":2211,"end":2215},"obj":"Body_part"}],"attributes":[{"id":"A30","pred":"uberon_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A31","pred":"uberon_id","subj":"T31","obj":"http://purl.obolibrary.org/obo/UBERON_0002405"},{"id":"A32","pred":"uberon_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/UBERON_0002371"},{"id":"A33","pred":"uberon_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A34","pred":"uberon_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A35","pred":"uberon_id","subj":"T35","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A36","pred":"uberon_id","subj":"T36","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A37","pred":"uberon_id","subj":"T37","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"5 Melatonin \u0026 immunomodulation\nWhen virus is inhaled and infects respiratory epithelial cells, dendritic cells phagocytose the virus and present antigens to T cells. Effector T cell function by killing the infected epithelial cells, and cytotoxic CD8+ T cells produce and release pro-inflammatory cytokines which induce cell apoptosis [46]. Both the pathogen (CoV) and cell apoptosis trigger and amplify the immune response. The exacerbation of cytokine production, excessive recruitment of immune cells and the uncontrollable epithelial damage generates a vicious circle for infection related ALI/ARDS [47]. The clinical characteristics of COVID-19 suggest that a reduced level of neutrophils, lymphocytes and CD8+ T cells in peripheral blood [7,48]. Melatonin exerts regulatory actions on the immune system and directly enhances the immune response by improving proliferation and maturation of natural killing cells, T and B lymphocytes, granulocytes and monocytes in both bone marrow and other tissues [49]. In macrophages, antigen presentation is also augmented after the application of melatonin, where the up-regulation of complement receptor 3, MHC class I and class II, and CD4 antigens were detected [50].\nNOD-like receptor 3 (NLRP3) inflammasome is part of the innate immune response during lung infection. The pathogen, including a virus (CoVs has not yet been tested), triggers NLRP3 activation to amplify the inflammation. There is probably a balance of the protective and damaging actions of NLRP3 in the lung. Thus, in a mouse experiment, inhibition of NLRP3 in the early phase of infection increased mortality, whereas suppression of NLRP3 at the peak of infection allowed for a protective effect [51]. This supports the use of melatonin in ALI/ARDS when inflammation is most severe. Inflammasome NLRP3 is correlated to lung diseases caused by infection, including influenza A virus, syncytial virus, and bacteria [[51], [52], [53]]. The efficacy of melatonin in regulating NLRP3 has been proven in radiation-induced lung injury, allergic airway inflammation and oxygen-induced ALI and LPS-induced ALI models, in which melatonin reduced the infiltration of macrophages and neutrophils into the lung in ALI due to the inhibition of NLRP3 inflammasome [4,28,54,55]."}

LitCovid_AGAC

{"project":"LitCovid_AGAC","denotations":[{"id":"p51326s19","span":{"begin":1411,"end":1418},"obj":"PosReg"}],"text":"5 Melatonin \u0026 immunomodulation\nWhen virus is inhaled and infects respiratory epithelial cells, dendritic cells phagocytose the virus and present antigens to T cells. Effector T cell function by killing the infected epithelial cells, and cytotoxic CD8+ T cells produce and release pro-inflammatory cytokines which induce cell apoptosis [46]. Both the pathogen (CoV) and cell apoptosis trigger and amplify the immune response. The exacerbation of cytokine production, excessive recruitment of immune cells and the uncontrollable epithelial damage generates a vicious circle for infection related ALI/ARDS [47]. The clinical characteristics of COVID-19 suggest that a reduced level of neutrophils, lymphocytes and CD8+ T cells in peripheral blood [7,48]. Melatonin exerts regulatory actions on the immune system and directly enhances the immune response by improving proliferation and maturation of natural killing cells, T and B lymphocytes, granulocytes and monocytes in both bone marrow and other tissues [49]. In macrophages, antigen presentation is also augmented after the application of melatonin, where the up-regulation of complement receptor 3, MHC class I and class II, and CD4 antigens were detected [50].\nNOD-like receptor 3 (NLRP3) inflammasome is part of the innate immune response during lung infection. The pathogen, including a virus (CoVs has not yet been tested), triggers NLRP3 activation to amplify the inflammation. There is probably a balance of the protective and damaging actions of NLRP3 in the lung. Thus, in a mouse experiment, inhibition of NLRP3 in the early phase of infection increased mortality, whereas suppression of NLRP3 at the peak of infection allowed for a protective effect [51]. This supports the use of melatonin in ALI/ARDS when inflammation is most severe. Inflammasome NLRP3 is correlated to lung diseases caused by infection, including influenza A virus, syncytial virus, and bacteria [[51], [52], [53]]. The efficacy of melatonin in regulating NLRP3 has been proven in radiation-induced lung injury, allergic airway inflammation and oxygen-induced ALI and LPS-induced ALI models, in which melatonin reduced the infiltration of macrophages and neutrophils into the lung in ALI due to the inhibition of NLRP3 inflammasome [4,28,54,55]."}

LitCovid-PD-MONDO

LitCovid-PD-CLO

LitCovid-PD-CHEBI

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T58","span":{"begin":326,"end":335},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T59","span":{"begin":326,"end":335},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T60","span":{"begin":375,"end":384},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T61","span":{"begin":375,"end":384},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T62","span":{"begin":409,"end":424},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T63","span":{"begin":446,"end":465},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T64","span":{"begin":836,"end":851},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T65","span":{"begin":1028,"end":1048},"obj":"http://purl.obolibrary.org/obo/GO_0019882"},{"id":"T66","span":{"begin":1116,"end":1126},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T67","span":{"begin":1272,"end":1294},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T68","span":{"begin":1279,"end":1294},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T69","span":{"begin":1423,"end":1435},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T70","span":{"begin":1772,"end":1784},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T71","span":{"begin":2063,"end":2075},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"5 Melatonin \u0026 immunomodulation\nWhen virus is inhaled and infects respiratory epithelial cells, dendritic cells phagocytose the virus and present antigens to T cells. Effector T cell function by killing the infected epithelial cells, and cytotoxic CD8+ T cells produce and release pro-inflammatory cytokines which induce cell apoptosis [46]. Both the pathogen (CoV) and cell apoptosis trigger and amplify the immune response. The exacerbation of cytokine production, excessive recruitment of immune cells and the uncontrollable epithelial damage generates a vicious circle for infection related ALI/ARDS [47]. The clinical characteristics of COVID-19 suggest that a reduced level of neutrophils, lymphocytes and CD8+ T cells in peripheral blood [7,48]. Melatonin exerts regulatory actions on the immune system and directly enhances the immune response by improving proliferation and maturation of natural killing cells, T and B lymphocytes, granulocytes and monocytes in both bone marrow and other tissues [49]. In macrophages, antigen presentation is also augmented after the application of melatonin, where the up-regulation of complement receptor 3, MHC class I and class II, and CD4 antigens were detected [50].\nNOD-like receptor 3 (NLRP3) inflammasome is part of the innate immune response during lung infection. The pathogen, including a virus (CoVs has not yet been tested), triggers NLRP3 activation to amplify the inflammation. There is probably a balance of the protective and damaging actions of NLRP3 in the lung. Thus, in a mouse experiment, inhibition of NLRP3 in the early phase of infection increased mortality, whereas suppression of NLRP3 at the peak of infection allowed for a protective effect [51]. This supports the use of melatonin in ALI/ARDS when inflammation is most severe. Inflammasome NLRP3 is correlated to lung diseases caused by infection, including influenza A virus, syncytial virus, and bacteria [[51], [52], [53]]. The efficacy of melatonin in regulating NLRP3 has been proven in radiation-induced lung injury, allergic airway inflammation and oxygen-induced ALI and LPS-induced ALI models, in which melatonin reduced the infiltration of macrophages and neutrophils into the lung in ALI due to the inhibition of NLRP3 inflammasome [4,28,54,55]."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T91","span":{"begin":0,"end":31},"obj":"Sentence"},{"id":"T92","span":{"begin":32,"end":166},"obj":"Sentence"},{"id":"T93","span":{"begin":167,"end":341},"obj":"Sentence"},{"id":"T94","span":{"begin":342,"end":425},"obj":"Sentence"},{"id":"T95","span":{"begin":426,"end":609},"obj":"Sentence"},{"id":"T96","span":{"begin":610,"end":752},"obj":"Sentence"},{"id":"T97","span":{"begin":753,"end":1011},"obj":"Sentence"},{"id":"T98","span":{"begin":1012,"end":1215},"obj":"Sentence"},{"id":"T99","span":{"begin":1216,"end":1317},"obj":"Sentence"},{"id":"T100","span":{"begin":1318,"end":1436},"obj":"Sentence"},{"id":"T101","span":{"begin":1437,"end":1525},"obj":"Sentence"},{"id":"T102","span":{"begin":1526,"end":1719},"obj":"Sentence"},{"id":"T103","span":{"begin":1720,"end":1800},"obj":"Sentence"},{"id":"T104","span":{"begin":1801,"end":1950},"obj":"Sentence"},{"id":"T105","span":{"begin":1951,"end":2280},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"5 Melatonin \u0026 immunomodulation\nWhen virus is inhaled and infects respiratory epithelial cells, dendritic cells phagocytose the virus and present antigens to T cells. Effector T cell function by killing the infected epithelial cells, and cytotoxic CD8+ T cells produce and release pro-inflammatory cytokines which induce cell apoptosis [46]. Both the pathogen (CoV) and cell apoptosis trigger and amplify the immune response. The exacerbation of cytokine production, excessive recruitment of immune cells and the uncontrollable epithelial damage generates a vicious circle for infection related ALI/ARDS [47]. The clinical characteristics of COVID-19 suggest that a reduced level of neutrophils, lymphocytes and CD8+ T cells in peripheral blood [7,48]. Melatonin exerts regulatory actions on the immune system and directly enhances the immune response by improving proliferation and maturation of natural killing cells, T and B lymphocytes, granulocytes and monocytes in both bone marrow and other tissues [49]. In macrophages, antigen presentation is also augmented after the application of melatonin, where the up-regulation of complement receptor 3, MHC class I and class II, and CD4 antigens were detected [50].\nNOD-like receptor 3 (NLRP3) inflammasome is part of the innate immune response during lung infection. The pathogen, including a virus (CoVs has not yet been tested), triggers NLRP3 activation to amplify the inflammation. There is probably a balance of the protective and damaging actions of NLRP3 in the lung. Thus, in a mouse experiment, inhibition of NLRP3 in the early phase of infection increased mortality, whereas suppression of NLRP3 at the peak of infection allowed for a protective effect [51]. This supports the use of melatonin in ALI/ARDS when inflammation is most severe. Inflammasome NLRP3 is correlated to lung diseases caused by infection, including influenza A virus, syncytial virus, and bacteria [[51], [52], [53]]. The efficacy of melatonin in regulating NLRP3 has been proven in radiation-induced lung injury, allergic airway inflammation and oxygen-induced ALI and LPS-induced ALI models, in which melatonin reduced the infiltration of macrophages and neutrophils into the lung in ALI due to the inhibition of NLRP3 inflammasome [4,28,54,55]."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T69","span":{"begin":595,"end":598},"obj":"Phenotype"},{"id":"T70","span":{"begin":1758,"end":1761},"obj":"Phenotype"},{"id":"T71","span":{"begin":1837,"end":1850},"obj":"Phenotype"},{"id":"T72","span":{"begin":2095,"end":2098},"obj":"Phenotype"},{"id":"T73","span":{"begin":2115,"end":2118},"obj":"Phenotype"},{"id":"T74","span":{"begin":2219,"end":2222},"obj":"Phenotype"}],"attributes":[{"id":"A69","pred":"hp_id","subj":"T69","obj":"http://www.orpha.net/ORDO/Orphanet_178320"},{"id":"A70","pred":"hp_id","subj":"T70","obj":"http://www.orpha.net/ORDO/Orphanet_178320"},{"id":"A71","pred":"hp_id","subj":"T71","obj":"http://purl.obolibrary.org/obo/HP_0002088"},{"id":"A72","pred":"hp_id","subj":"T72","obj":"http://www.orpha.net/ORDO/Orphanet_178320"},{"id":"A73","pred":"hp_id","subj":"T73","obj":"http://www.orpha.net/ORDO/Orphanet_178320"},{"id":"A74","pred":"hp_id","subj":"T74","obj":"http://www.orpha.net/ORDO/Orphanet_178320"}],"text":"5 Melatonin \u0026 immunomodulation\nWhen virus is inhaled and infects respiratory epithelial cells, dendritic cells phagocytose the virus and present antigens to T cells. Effector T cell function by killing the infected epithelial cells, and cytotoxic CD8+ T cells produce and release pro-inflammatory cytokines which induce cell apoptosis [46]. Both the pathogen (CoV) and cell apoptosis trigger and amplify the immune response. The exacerbation of cytokine production, excessive recruitment of immune cells and the uncontrollable epithelial damage generates a vicious circle for infection related ALI/ARDS [47]. The clinical characteristics of COVID-19 suggest that a reduced level of neutrophils, lymphocytes and CD8+ T cells in peripheral blood [7,48]. Melatonin exerts regulatory actions on the immune system and directly enhances the immune response by improving proliferation and maturation of natural killing cells, T and B lymphocytes, granulocytes and monocytes in both bone marrow and other tissues [49]. In macrophages, antigen presentation is also augmented after the application of melatonin, where the up-regulation of complement receptor 3, MHC class I and class II, and CD4 antigens were detected [50].\nNOD-like receptor 3 (NLRP3) inflammasome is part of the innate immune response during lung infection. The pathogen, including a virus (CoVs has not yet been tested), triggers NLRP3 activation to amplify the inflammation. There is probably a balance of the protective and damaging actions of NLRP3 in the lung. Thus, in a mouse experiment, inhibition of NLRP3 in the early phase of infection increased mortality, whereas suppression of NLRP3 at the peak of infection allowed for a protective effect [51]. This supports the use of melatonin in ALI/ARDS when inflammation is most severe. Inflammasome NLRP3 is correlated to lung diseases caused by infection, including influenza A virus, syncytial virus, and bacteria [[51], [52], [53]]. The efficacy of melatonin in regulating NLRP3 has been proven in radiation-induced lung injury, allergic airway inflammation and oxygen-induced ALI and LPS-induced ALI models, in which melatonin reduced the infiltration of macrophages and neutrophils into the lung in ALI due to the inhibition of NLRP3 inflammasome [4,28,54,55]."}

2_test

{"project":"2_test","denotations":[{"id":"32217117-30052492-66453504","span":{"begin":337,"end":339},"obj":"30052492"},{"id":"32217117-16623752-66453505","span":{"begin":1007,"end":1009},"obj":"16623752"},{"id":"32217117-10231729-66453506","span":{"begin":1211,"end":1213},"obj":"10231729"},{"id":"32217117-27283237-66453507","span":{"begin":1715,"end":1717},"obj":"27283237"},{"id":"32217117-27283237-66453508","span":{"begin":1933,"end":1935},"obj":"27283237"},{"id":"32217117-32047436-66453509","span":{"begin":1939,"end":1941},"obj":"32047436"},{"id":"32217117-17803352-66453510","span":{"begin":1945,"end":1947},"obj":"17803352"},{"id":"32217117-25491480-66453511","span":{"begin":2270,"end":2272},"obj":"25491480"},{"id":"32217117-31738882-66453512","span":{"begin":2273,"end":2275},"obj":"31738882"},{"id":"32217117-26888116-66453513","span":{"begin":2276,"end":2278},"obj":"26888116"}],"text":"5 Melatonin \u0026 immunomodulation\nWhen virus is inhaled and infects respiratory epithelial cells, dendritic cells phagocytose the virus and present antigens to T cells. Effector T cell function by killing the infected epithelial cells, and cytotoxic CD8+ T cells produce and release pro-inflammatory cytokines which induce cell apoptosis [46]. Both the pathogen (CoV) and cell apoptosis trigger and amplify the immune response. The exacerbation of cytokine production, excessive recruitment of immune cells and the uncontrollable epithelial damage generates a vicious circle for infection related ALI/ARDS [47]. The clinical characteristics of COVID-19 suggest that a reduced level of neutrophils, lymphocytes and CD8+ T cells in peripheral blood [7,48]. Melatonin exerts regulatory actions on the immune system and directly enhances the immune response by improving proliferation and maturation of natural killing cells, T and B lymphocytes, granulocytes and monocytes in both bone marrow and other tissues [49]. In macrophages, antigen presentation is also augmented after the application of melatonin, where the up-regulation of complement receptor 3, MHC class I and class II, and CD4 antigens were detected [50].\nNOD-like receptor 3 (NLRP3) inflammasome is part of the innate immune response during lung infection. The pathogen, including a virus (CoVs has not yet been tested), triggers NLRP3 activation to amplify the inflammation. There is probably a balance of the protective and damaging actions of NLRP3 in the lung. Thus, in a mouse experiment, inhibition of NLRP3 in the early phase of infection increased mortality, whereas suppression of NLRP3 at the peak of infection allowed for a protective effect [51]. This supports the use of melatonin in ALI/ARDS when inflammation is most severe. Inflammasome NLRP3 is correlated to lung diseases caused by infection, including influenza A virus, syncytial virus, and bacteria [[51], [52], [53]]. The efficacy of melatonin in regulating NLRP3 has been proven in radiation-induced lung injury, allergic airway inflammation and oxygen-induced ALI and LPS-induced ALI models, in which melatonin reduced the infiltration of macrophages and neutrophils into the lung in ALI due to the inhibition of NLRP3 inflammasome [4,28,54,55]."}

PMC:7102583 / 13133-15413 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7102583 / 13133-15413 JSON TXT