PMC:7321036 / 53653-54985 JSONTXT

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    LitCovid-PMC-OGER-BB

    {"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T173","span":{"begin":796,"end":922},"obj":"GO:0065007"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    LitCovid-PD-FMA-UBERON

    {"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T426","span":{"begin":121,"end":129},"obj":"Body_part"},{"id":"T427","span":{"begin":186,"end":191},"obj":"Body_part"},{"id":"T428","span":{"begin":454,"end":463},"obj":"Body_part"},{"id":"T429","span":{"begin":737,"end":746},"obj":"Body_part"},{"id":"T430","span":{"begin":1151,"end":1159},"obj":"Body_part"}],"attributes":[{"id":"A426","pred":"fma_id","subj":"T426","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A427","pred":"fma_id","subj":"T427","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A428","pred":"fma_id","subj":"T428","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A429","pred":"fma_id","subj":"T429","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A430","pred":"fma_id","subj":"T430","obj":"http://purl.org/sig/ont/fma/fma84050"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    LitCovid-PD-MONDO

    {"project":"LitCovid-PD-MONDO","denotations":[{"id":"T272","span":{"begin":166,"end":174},"obj":"Disease"},{"id":"T273","span":{"begin":279,"end":290},"obj":"Disease"},{"id":"T274","span":{"begin":318,"end":326},"obj":"Disease"},{"id":"T275","span":{"begin":484,"end":500},"obj":"Disease"},{"id":"T276","span":{"begin":613,"end":625},"obj":"Disease"},{"id":"T277","span":{"begin":766,"end":782},"obj":"Disease"},{"id":"T278","span":{"begin":794,"end":802},"obj":"Disease"},{"id":"T279","span":{"begin":804,"end":810},"obj":"Disease"},{"id":"T280","span":{"begin":822,"end":831},"obj":"Disease"},{"id":"T281","span":{"begin":1067,"end":1076},"obj":"Disease"},{"id":"T282","span":{"begin":1098,"end":1106},"obj":"Disease"},{"id":"T283","span":{"begin":1109,"end":1118},"obj":"Disease"},{"id":"T284","span":{"begin":1310,"end":1318},"obj":"Disease"}],"attributes":[{"id":"A272","pred":"mondo_id","subj":"T272","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A273","pred":"mondo_id","subj":"T273","obj":"http://purl.obolibrary.org/obo/MONDO_0003783"},{"id":"A274","pred":"mondo_id","subj":"T274","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A275","pred":"mondo_id","subj":"T275","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A276","pred":"mondo_id","subj":"T276","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"},{"id":"A277","pred":"mondo_id","subj":"T277","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A278","pred":"mondo_id","subj":"T278","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A279","pred":"mondo_id","subj":"T279","obj":"http://purl.obolibrary.org/obo/MONDO_0005502"},{"id":"A280","pred":"mondo_id","subj":"T280","obj":"http://purl.obolibrary.org/obo/MONDO_0005812"},{"id":"A281","pred":"mondo_id","subj":"T281","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A282","pred":"mondo_id","subj":"T282","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A283","pred":"mondo_id","subj":"T283","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A284","pred":"mondo_id","subj":"T284","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    LitCovid-PD-CLO

    {"project":"LitCovid-PD-CLO","denotations":[{"id":"T721","span":{"begin":35,"end":43},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T722","span":{"begin":186,"end":191},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T723","span":{"begin":508,"end":509},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T724","span":{"begin":519,"end":528},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T725","span":{"begin":681,"end":690},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T726","span":{"begin":811,"end":816},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T727","span":{"begin":832,"end":833},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T728","span":{"begin":834,"end":839},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T729","span":{"begin":903,"end":907},"obj":"http://purl.obolibrary.org/obo/CLO_0001185"},{"id":"T730","span":{"begin":998,"end":1003},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T731","span":{"begin":1205,"end":1206},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    LitCovid-PD-CHEBI

    {"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T49049","span":{"begin":252,"end":254},"obj":"Chemical"},{"id":"T90781","span":{"begin":258,"end":260},"obj":"Chemical"},{"id":"T28144","span":{"begin":347,"end":349},"obj":"Chemical"}],"attributes":[{"id":"A5102","pred":"chebi_id","subj":"T49049","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A99469","pred":"chebi_id","subj":"T49049","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A85893","pred":"chebi_id","subj":"T90781","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A90821","pred":"chebi_id","subj":"T90781","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A18323","pred":"chebi_id","subj":"T28144","obj":"http://purl.obolibrary.org/obo/CHEBI_49648"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    LitCovid-PD-GO-BP

    {"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T388","span":{"begin":30,"end":34},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T389","span":{"begin":85,"end":89},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T390","span":{"begin":121,"end":140},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T391","span":{"begin":145,"end":162},"obj":"http://purl.obolibrary.org/obo/GO_0019079"},{"id":"T392","span":{"begin":145,"end":162},"obj":"http://purl.obolibrary.org/obo/GO_0019058"},{"id":"T393","span":{"begin":365,"end":369},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T394","span":{"begin":484,"end":500},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T395","span":{"begin":510,"end":528},"obj":"http://purl.obolibrary.org/obo/GO_0051403"},{"id":"T396","span":{"begin":514,"end":528},"obj":"http://purl.obolibrary.org/obo/GO_0000165"},{"id":"T397","span":{"begin":514,"end":518},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T398","span":{"begin":519,"end":528},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T399","span":{"begin":580,"end":590},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T400","span":{"begin":613,"end":625},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T401","span":{"begin":672,"end":690},"obj":"http://purl.obolibrary.org/obo/GO_0051403"},{"id":"T402","span":{"begin":676,"end":690},"obj":"http://purl.obolibrary.org/obo/GO_0000165"},{"id":"T403","span":{"begin":676,"end":680},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T404","span":{"begin":681,"end":690},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T405","span":{"begin":766,"end":782},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T406","span":{"begin":954,"end":958},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T407","span":{"begin":1044,"end":1059},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T408","span":{"begin":1124,"end":1128},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T409","span":{"begin":1151,"end":1170},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T410","span":{"begin":1184,"end":1201},"obj":"http://purl.obolibrary.org/obo/GO_0019079"},{"id":"T411","span":{"begin":1184,"end":1201},"obj":"http://purl.obolibrary.org/obo/GO_0019058"},{"id":"T412","span":{"begin":1252,"end":1256},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T413","span":{"begin":1319,"end":1331},"obj":"http://purl.obolibrary.org/obo/GO_0009405"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    LitCovid-PD-HP

    {"project":"LitCovid-PD-HP","denotations":[{"id":"T11","span":{"begin":279,"end":290},"obj":"Phenotype"}],"attributes":[{"id":"A11","pred":"hp_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/HP_0001888"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    LitCovid-PubTator

    {"project":"LitCovid-PubTator","denotations":[{"id":"1200","span":{"begin":26,"end":29},"obj":"Gene"},{"id":"1201","span":{"begin":81,"end":89},"obj":"Gene"},{"id":"1202","span":{"begin":252,"end":256},"obj":"Gene"},{"id":"1203","span":{"begin":258,"end":263},"obj":"Gene"},{"id":"1204","span":{"begin":269,"end":274},"obj":"Gene"},{"id":"1205","span":{"begin":361,"end":364},"obj":"Gene"},{"id":"1206","span":{"begin":510,"end":518},"obj":"Gene"},{"id":"1207","span":{"begin":672,"end":680},"obj":"Gene"},{"id":"1208","span":{"begin":950,"end":958},"obj":"Gene"},{"id":"1209","span":{"begin":1120,"end":1128},"obj":"Gene"},{"id":"1210","span":{"begin":1248,"end":1251},"obj":"Gene"},{"id":"1211","span":{"begin":794,"end":802},"obj":"Species"},{"id":"1212","span":{"begin":804,"end":816},"obj":"Species"},{"id":"1213","span":{"begin":822,"end":839},"obj":"Species"},{"id":"1214","span":{"begin":863,"end":867},"obj":"Species"},{"id":"1215","span":{"begin":166,"end":185},"obj":"Disease"},{"id":"1216","span":{"begin":279,"end":290},"obj":"Disease"},{"id":"1217","span":{"begin":318,"end":326},"obj":"Disease"},{"id":"1218","span":{"begin":484,"end":500},"obj":"Disease"},{"id":"1219","span":{"begin":613,"end":625},"obj":"Disease"},{"id":"1220","span":{"begin":766,"end":782},"obj":"Disease"},{"id":"1221","span":{"begin":1067,"end":1076},"obj":"Disease"},{"id":"1222","span":{"begin":1098,"end":1118},"obj":"Disease"},{"id":"1223","span":{"begin":1310,"end":1318},"obj":"Disease"}],"attributes":[{"id":"A1200","pred":"tao:has_database_id","subj":"1200","obj":"Gene:5594"},{"id":"A1201","pred":"tao:has_database_id","subj":"1201","obj":"Gene:5594"},{"id":"A1202","pred":"tao:has_database_id","subj":"1202","obj":"Gene:3569"},{"id":"A1203","pred":"tao:has_database_id","subj":"1203","obj":"Gene:3586"},{"id":"A1204","pred":"tao:has_database_id","subj":"1204","obj":"Gene:7124"},{"id":"A1205","pred":"tao:has_database_id","subj":"1205","obj":"Gene:5594"},{"id":"A1206","pred":"tao:has_database_id","subj":"1206","obj":"Gene:5594"},{"id":"A1207","pred":"tao:has_database_id","subj":"1207","obj":"Gene:5594"},{"id":"A1208","pred":"tao:has_database_id","subj":"1208","obj":"Gene:26416"},{"id":"A1209","pred":"tao:has_database_id","subj":"1209","obj":"Gene:5594"},{"id":"A1210","pred":"tao:has_database_id","subj":"1210","obj":"Gene:5594"},{"id":"A1211","pred":"tao:has_database_id","subj":"1211","obj":"Tax:694009"},{"id":"A1212","pred":"tao:has_database_id","subj":"1212","obj":"Tax:12637"},{"id":"A1213","pred":"tao:has_database_id","subj":"1213","obj":"Tax:11320"},{"id":"A1214","pred":"tao:has_database_id","subj":"1214","obj":"Tax:10090"},{"id":"A1215","pred":"tao:has_database_id","subj":"1215","obj":"MESH:C000657245"},{"id":"A1216","pred":"tao:has_database_id","subj":"1216","obj":"MESH:D008231"},{"id":"A1217","pred":"tao:has_database_id","subj":"1217","obj":"MESH:C000657245"},{"id":"A1218","pred":"tao:has_database_id","subj":"1218","obj":"MESH:D001102"},{"id":"A1219","pred":"tao:has_database_id","subj":"1219","obj":"MESH:D007249"},{"id":"A1220","pred":"tao:has_database_id","subj":"1220","obj":"MESH:D001102"},{"id":"A1221","pred":"tao:has_database_id","subj":"1221","obj":"MESH:D007239"},{"id":"A1222","pred":"tao:has_database_id","subj":"1222","obj":"MESH:C000657245"},{"id":"A1223","pred":"tao:has_database_id","subj":"1223","obj":"MESH:C000657245"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    LitCovid-sentences

    {"project":"LitCovid-sentences","denotations":[{"id":"T351","span":{"begin":0,"end":192},"obj":"Sentence"},{"id":"T352","span":{"begin":193,"end":356},"obj":"Sentence"},{"id":"T353","span":{"begin":357,"end":464},"obj":"Sentence"},{"id":"T354","span":{"begin":465,"end":657},"obj":"Sentence"},{"id":"T355","span":{"begin":658,"end":940},"obj":"Sentence"},{"id":"T356","span":{"begin":941,"end":1077},"obj":"Sentence"},{"id":"T357","span":{"begin":1078,"end":1332},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}

    2_test

    {"project":"2_test","denotations":[{"id":"32645325-32217834-20773089","span":{"begin":350,"end":354},"obj":"32217834"},{"id":"32645325-25131378-20773090","span":{"begin":880,"end":884},"obj":"25131378"},{"id":"32645325-29458547-20773091","span":{"begin":903,"end":907},"obj":"29458547"},{"id":"32645325-25122212-20773092","span":{"begin":934,"end":938},"obj":"25122212"}],"text":"The predicted increase in p38/MAPK activity led us to investigate the effects of p38/MAPK inhibition on pro-inflammatory cytokine production and viral replication in SARS-CoV-2-infected cells. Recent immunological studies have indicated that increased IL-6, IL-10, and TNF-α and lymphopenia are associated with severe COVID-19 cases (Pedersen and Ho 2020). The p38/MAPK pathway responds to and controls production of potentially harmful pro-inflammatory cytokines. Several pathogenic viral infections induce a p38/MAPK signaling state that exhibits uncontrolled positive feedback regulation, leading to excessive inflammation associated with severe disease. Inhibition of p38/MAPK signaling suppressed the overproduction of inflammatory cytokines induced by several viral infections, including SARS-CoV, Dengue virus, and influenza A virus, improving survival in mice (Fu et al., 2014; Growcott et al., 2018; Jimenez-Guardeño et al., 2014). However, p38/MAPK inhibition did not directly impair the virus in these cases but, instead, the host’s immune response to the infection. In contrast, during SARS-CoV-2 infection, p38/MAPK inhibition suppressed cytokine production and impaired viral replication by a still unknown mechanism, suggesting that p38/MAPK inhibition may target multiple mechanisms related to COVID-19 pathogenesis."}