PMC:7381711 / 14864-16223 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T122","span":{"begin":58,"end":65},"obj":"Body_part"},{"id":"T123","span":{"begin":421,"end":430},"obj":"Body_part"},{"id":"T124","span":{"begin":457,"end":465},"obj":"Body_part"},{"id":"T125","span":{"begin":509,"end":513},"obj":"Body_part"},{"id":"T126","span":{"begin":509,"end":511},"obj":"Body_part"},{"id":"T127","span":{"begin":516,"end":518},"obj":"Body_part"},{"id":"T128","span":{"begin":526,"end":528},"obj":"Body_part"},{"id":"T129","span":{"begin":541,"end":548},"obj":"Body_part"},{"id":"T130","span":{"begin":626,"end":643},"obj":"Body_part"},{"id":"T131","span":{"begin":638,"end":643},"obj":"Body_part"},{"id":"T132","span":{"begin":654,"end":663},"obj":"Body_part"},{"id":"T133","span":{"begin":693,"end":700},"obj":"Body_part"},{"id":"T134","span":{"begin":925,"end":929},"obj":"Body_part"},{"id":"T135","span":{"begin":1016,"end":1023},"obj":"Body_part"},{"id":"T136","span":{"begin":1060,"end":1077},"obj":"Body_part"},{"id":"T137","span":{"begin":1072,"end":1077},"obj":"Body_part"},{"id":"T138","span":{"begin":1123,"end":1136},"obj":"Body_part"},{"id":"T139","span":{"begin":1162,"end":1172},"obj":"Body_part"},{"id":"T140","span":{"begin":1204,"end":1211},"obj":"Body_part"}],"attributes":[{"id":"A122","pred":"fma_id","subj":"T122","obj":"http://purl.org/sig/ont/fma/fma82839"},{"id":"A123","pred":"fma_id","subj":"T123","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A124","pred":"fma_id","subj":"T124","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A125","pred":"fma_id","subj":"T125","obj":"http://purl.org/sig/ont/fma/fma86583"},{"id":"A126","pred":"fma_id","subj":"T126","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A127","pred":"fma_id","subj":"T127","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A128","pred":"fma_id","subj":"T128","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A129","pred":"fma_id","subj":"T129","obj":"http://purl.org/sig/ont/fma/fma82839"},{"id":"A130","pred":"fma_id","subj":"T130","obj":"http://purl.org/sig/ont/fma/fma66772"},{"id":"A131","pred":"fma_id","subj":"T131","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A132","pred":"fma_id","subj":"T132","obj":"http://purl.org/sig/ont/fma/fma62864"},{"id":"A133","pred":"fma_id","subj":"T133","obj":"http://purl.org/sig/ont/fma/fma82839"},{"id":"A134","pred":"fma_id","subj":"T134","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A135","pred":"fma_id","subj":"T135","obj":"http://purl.org/sig/ont/fma/fma82839"},{"id":"A136","pred":"fma_id","subj":"T136","obj":"http://purl.org/sig/ont/fma/fma66772"},{"id":"A137","pred":"fma_id","subj":"T137","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A138","pred":"fma_id","subj":"T138","obj":"http://purl.org/sig/ont/fma/fma9825"},{"id":"A139","pred":"fma_id","subj":"T139","obj":"http://purl.org/sig/ont/fma/fma62860"},{"id":"A140","pred":"fma_id","subj":"T140","obj":"http://purl.org/sig/ont/fma/fma82839"}],"text":"There are innumerable studies that have demonstrated that heparin can dampen inflammation through its interaction with key inflammatory mediators. The proinflammatory transcription factor nuclear factor-κB (NF-κB), which has been found to be involved in the pathogenesis of SARS-CoV, the virus underlying the 2003 severe acute respiratory syndrome (SARS) epidemic (16), leads to the production of downstream inflammatory cytokines and other immune response proteins including tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 (13, 47). Heparin has been observed to directly dampen NF-κB signaling in LPS-stimulated human endothelial cells and human monocytes (21). Similarly, a synthetic heparin-like drug has recently been developed that neutralizes high mobility group box 1 (HMGB1; 5), a proinflammatory mediator that is known to play a role in the pathogenesis of viral infections (15). With respect to inflammatory cell infiltration, a phenomenon that has been observed pathologically in COVID-19 (2, 39), heparin can directly interact with vascular endothelial cells leading to reduced recruitment of the innate immune system and direct inhibition of neutrophil activation (13). More broadly, heparin has been shown to dampen inflammation in other preclinical models characterized by robust inflammation including pancreatitis (12) and sepsis (33)."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T11","span":{"begin":1123,"end":1136},"obj":"Body_part"}],"attributes":[{"id":"A11","pred":"uberon_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/UBERON_0002405"}],"text":"There are innumerable studies that have demonstrated that heparin can dampen inflammation through its interaction with key inflammatory mediators. The proinflammatory transcription factor nuclear factor-κB (NF-κB), which has been found to be involved in the pathogenesis of SARS-CoV, the virus underlying the 2003 severe acute respiratory syndrome (SARS) epidemic (16), leads to the production of downstream inflammatory cytokines and other immune response proteins including tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 (13, 47). Heparin has been observed to directly dampen NF-κB signaling in LPS-stimulated human endothelial cells and human monocytes (21). Similarly, a synthetic heparin-like drug has recently been developed that neutralizes high mobility group box 1 (HMGB1; 5), a proinflammatory mediator that is known to play a role in the pathogenesis of viral infections (15). With respect to inflammatory cell infiltration, a phenomenon that has been observed pathologically in COVID-19 (2, 39), heparin can directly interact with vascular endothelial cells leading to reduced recruitment of the innate immune system and direct inhibition of neutrophil activation (13). More broadly, heparin has been shown to dampen inflammation in other preclinical models characterized by robust inflammation including pancreatitis (12) and sepsis (33)."}

{"project":"LitCovid-PubTator","denotations":[{"id":"547","span":{"begin":476,"end":499},"obj":"Gene"},{"id":"548","span":{"begin":501,"end":506},"obj":"Gene"},{"id":"549","span":{"begin":509,"end":514},"obj":"Gene"},{"id":"550","span":{"begin":516,"end":520},"obj":"Gene"},{"id":"551","span":{"begin":526,"end":530},"obj":"Gene"},{"id":"552","span":{"begin":756,"end":781},"obj":"Gene"},{"id":"553","span":{"begin":783,"end":788},"obj":"Gene"},{"id":"554","span":{"begin":274,"end":282},"obj":"Species"},{"id":"555","span":{"begin":620,"end":625},"obj":"Species"},{"id":"556","span":{"begin":648,"end":653},"obj":"Species"},{"id":"557","span":{"begin":58,"end":65},"obj":"Chemical"},{"id":"558","span":{"begin":541,"end":548},"obj":"Chemical"},{"id":"559","span":{"begin":605,"end":608},"obj":"Chemical"},{"id":"560","span":{"begin":693,"end":700},"obj":"Chemical"},{"id":"561","span":{"begin":1016,"end":1023},"obj":"Chemical"},{"id":"562","span":{"begin":1204,"end":1211},"obj":"Chemical"},{"id":"563","span":{"begin":77,"end":89},"obj":"Disease"},{"id":"564","span":{"begin":873,"end":889},"obj":"Disease"},{"id":"565","span":{"begin":998,"end":1006},"obj":"Disease"},{"id":"566","span":{"begin":1237,"end":1249},"obj":"Disease"},{"id":"567","span":{"begin":1302,"end":1314},"obj":"Disease"},{"id":"568","span":{"begin":1325,"end":1337},"obj":"Disease"},{"id":"569","span":{"begin":1347,"end":1353},"obj":"Disease"}],"attributes":[{"id":"A547","pred":"tao:has_database_id","subj":"547","obj":"Gene:7124"},{"id":"A548","pred":"tao:has_database_id","subj":"548","obj":"Gene:7124"},{"id":"A549","pred":"tao:has_database_id","subj":"549","obj":"Gene:3552"},{"id":"A550","pred":"tao:has_database_id","subj":"550","obj":"Gene:3569"},{"id":"A551","pred":"tao:has_database_id","subj":"551","obj":"Gene:3576"},{"id":"A552","pred":"tao:has_database_id","subj":"552","obj":"Gene:3146"},{"id":"A553","pred":"tao:has_database_id","subj":"553","obj":"Gene:3146"},{"id":"A554","pred":"tao:has_database_id","subj":"554","obj":"Tax:694009"},{"id":"A555","pred":"tao:has_database_id","subj":"555","obj":"Tax:9606"},{"id":"A556","pred":"tao:has_database_id","subj":"556","obj":"Tax:9606"},{"id":"A557","pred":"tao:has_database_id","subj":"557","obj":"MESH:D006493"},{"id":"A558","pred":"tao:has_database_id","subj":"558","obj":"MESH:D006493"},{"id":"A559","pred":"tao:has_database_id","subj":"559","obj":"MESH:D008070"},{"id":"A560","pred":"tao:has_database_id","subj":"560","obj":"MESH:D006493"},{"id":"A561","pred":"tao:has_database_id","subj":"561","obj":"MESH:D006493"},{"id":"A562","pred":"tao:has_database_id","subj":"562","obj":"MESH:D006493"},{"id":"A563","pred":"tao:has_database_id","subj":"563","obj":"MESH:D007249"},{"id":"A564","pred":"tao:has_database_id","subj":"564","obj":"MESH:D001102"},{"id":"A565","pred":"tao:has_database_id","subj":"565","obj":"MESH:C000657245"},{"id":"A566","pred":"tao:has_database_id","subj":"566","obj":"MESH:D007249"},{"id":"A567","pred":"tao:has_database_id","subj":"567","obj":"MESH:D007249"},{"id":"A568","pred":"tao:has_database_id","subj":"568","obj":"MESH:D010195"},{"id":"A569","pred":"tao:has_database_id","subj":"569","obj":"MESH:D018805"}],"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":"There are innumerable studies that have demonstrated that heparin can dampen inflammation through its interaction with key inflammatory mediators. The proinflammatory transcription factor nuclear factor-κB (NF-κB), which has been found to be involved in the pathogenesis of SARS-CoV, the virus underlying the 2003 severe acute respiratory syndrome (SARS) epidemic (16), leads to the production of downstream inflammatory cytokines and other immune response proteins including tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 (13, 47). Heparin has been observed to directly dampen NF-κB signaling in LPS-stimulated human endothelial cells and human monocytes (21). Similarly, a synthetic heparin-like drug has recently been developed that neutralizes high mobility group box 1 (HMGB1; 5), a proinflammatory mediator that is known to play a role in the pathogenesis of viral infections (15). With respect to inflammatory cell infiltration, a phenomenon that has been observed pathologically in COVID-19 (2, 39), heparin can directly interact with vascular endothelial cells leading to reduced recruitment of the innate immune system and direct inhibition of neutrophil activation (13). More broadly, heparin has been shown to dampen inflammation in other preclinical models characterized by robust inflammation including pancreatitis (12) and sepsis (33)."}

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{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T171","span":{"begin":58,"end":65},"obj":"Chemical"},{"id":"T172","span":{"begin":207,"end":209},"obj":"Chemical"},{"id":"T175","span":{"begin":457,"end":465},"obj":"Chemical"},{"id":"T176","span":{"begin":509,"end":511},"obj":"Chemical"},{"id":"T178","span":{"begin":516,"end":518},"obj":"Chemical"},{"id":"T180","span":{"begin":526,"end":528},"obj":"Chemical"},{"id":"T182","span":{"begin":541,"end":548},"obj":"Chemical"},{"id":"T183","span":{"begin":586,"end":588},"obj":"Chemical"},{"id":"T186","span":{"begin":605,"end":608},"obj":"Chemical"},{"id":"T189","span":{"begin":693,"end":700},"obj":"Chemical"},{"id":"T190","span":{"begin":706,"end":710},"obj":"Chemical"},{"id":"T191","span":{"begin":770,"end":775},"obj":"Chemical"},{"id":"T192","span":{"begin":1016,"end":1023},"obj":"Chemical"},{"id":"T193","span":{"begin":1204,"end":1211},"obj":"Chemical"}],"attributes":[{"id":"A171","pred":"chebi_id","subj":"T171","obj":"http://purl.obolibrary.org/obo/CHEBI_28304"},{"id":"A172","pred":"chebi_id","subj":"T172","obj":"http://purl.obolibrary.org/obo/CHEBI_141424"},{"id":"A173","pred":"chebi_id","subj":"T172","obj":"http://purl.obolibrary.org/obo/CHEBI_25573"},{"id":"A174","pred":"chebi_id","subj":"T172","obj":"http://purl.obolibrary.org/obo/CHEBI_1224"},{"id":"A175","pred":"chebi_id","subj":"T175","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A176","pred":"chebi_id","subj":"T176","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A177","pred":"chebi_id","subj":"T176","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A178","pred":"chebi_id","subj":"T178","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A179","pred":"chebi_id","subj":"T178","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A180","pred":"chebi_id","subj":"T180","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A181","pred":"chebi_id","subj":"T180","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A182","pred":"chebi_id","subj":"T182","obj":"http://purl.obolibrary.org/obo/CHEBI_28304"},{"id":"A183","pred":"chebi_id","subj":"T183","obj":"http://purl.obolibrary.org/obo/CHEBI_141424"},{"id":"A184","pred":"chebi_id","subj":"T183","obj":"http://purl.obolibrary.org/obo/CHEBI_25573"},{"id":"A185","pred":"chebi_id","subj":"T183","obj":"http://purl.obolibrary.org/obo/CHEBI_1224"},{"id":"A186","pred":"chebi_id","subj":"T186","obj":"http://purl.obolibrary.org/obo/CHEBI_16412"},{"id":"A187","pred":"chebi_id","subj":"T186","obj":"http://purl.obolibrary.org/obo/CHEBI_52603"},{"id":"A188","pred":"chebi_id","subj":"T186","obj":"http://purl.obolibrary.org/obo/CHEBI_89981"},{"id":"A189","pred":"chebi_id","subj":"T189","obj":"http://purl.obolibrary.org/obo/CHEBI_28304"},{"id":"A190","pred":"chebi_id","subj":"T190","obj":"http://purl.obolibrary.org/obo/CHEBI_23888"},{"id":"A191","pred":"chebi_id","subj":"T191","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"},{"id":"A192","pred":"chebi_id","subj":"T192","obj":"http://purl.obolibrary.org/obo/CHEBI_28304"},{"id":"A193","pred":"chebi_id","subj":"T193","obj":"http://purl.obolibrary.org/obo/CHEBI_28304"}],"text":"There are innumerable studies that have demonstrated that heparin can dampen inflammation through its interaction with key inflammatory mediators. The proinflammatory transcription factor nuclear factor-κB (NF-κB), which has been found to be involved in the pathogenesis of SARS-CoV, the virus underlying the 2003 severe acute respiratory syndrome (SARS) epidemic (16), leads to the production of downstream inflammatory cytokines and other immune response proteins including tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 (13, 47). Heparin has been observed to directly dampen NF-κB signaling in LPS-stimulated human endothelial cells and human monocytes (21). Similarly, a synthetic heparin-like drug has recently been developed that neutralizes high mobility group box 1 (HMGB1; 5), a proinflammatory mediator that is known to play a role in the pathogenesis of viral infections (15). With respect to inflammatory cell infiltration, a phenomenon that has been observed pathologically in COVID-19 (2, 39), heparin can directly interact with vascular endothelial cells leading to reduced recruitment of the innate immune system and direct inhibition of neutrophil activation (13). More broadly, heparin has been shown to dampen inflammation in other preclinical models characterized by robust inflammation including pancreatitis (12) and sepsis (33)."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T17","span":{"begin":77,"end":89},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T18","span":{"begin":167,"end":187},"obj":"http://purl.obolibrary.org/obo/GO_0000981"},{"id":"T19","span":{"begin":167,"end":180},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T20","span":{"begin":258,"end":270},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T21","span":{"begin":441,"end":456},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T22","span":{"begin":482,"end":490},"obj":"http://purl.obolibrary.org/obo/GO_0070265"},{"id":"T23","span":{"begin":482,"end":490},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T24","span":{"begin":482,"end":490},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T25","span":{"begin":482,"end":490},"obj":"http://purl.obolibrary.org/obo/GO_0001906"},{"id":"T26","span":{"begin":592,"end":601},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T27","span":{"begin":857,"end":869},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T28","span":{"begin":873,"end":889},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T29","span":{"begin":1116,"end":1129},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T30","span":{"begin":1148,"end":1183},"obj":"http://purl.obolibrary.org/obo/GO_1902564"},{"id":"T31","span":{"begin":1162,"end":1183},"obj":"http://purl.obolibrary.org/obo/GO_0042119"},{"id":"T32","span":{"begin":1237,"end":1249},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T33","span":{"begin":1302,"end":1314},"obj":"http://purl.obolibrary.org/obo/GO_0006954"}],"text":"There are innumerable studies that have demonstrated that heparin can dampen inflammation through its interaction with key inflammatory mediators. The proinflammatory transcription factor nuclear factor-κB (NF-κB), which has been found to be involved in the pathogenesis of SARS-CoV, the virus underlying the 2003 severe acute respiratory syndrome (SARS) epidemic (16), leads to the production of downstream inflammatory cytokines and other immune response proteins including tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 (13, 47). Heparin has been observed to directly dampen NF-κB signaling in LPS-stimulated human endothelial cells and human monocytes (21). Similarly, a synthetic heparin-like drug has recently been developed that neutralizes high mobility group box 1 (HMGB1; 5), a proinflammatory mediator that is known to play a role in the pathogenesis of viral infections (15). With respect to inflammatory cell infiltration, a phenomenon that has been observed pathologically in COVID-19 (2, 39), heparin can directly interact with vascular endothelial cells leading to reduced recruitment of the innate immune system and direct inhibition of neutrophil activation (13). More broadly, heparin has been shown to dampen inflammation in other preclinical models characterized by robust inflammation including pancreatitis (12) and sepsis (33)."}

{"project":"LitCovid-sentences","denotations":[{"id":"T92","span":{"begin":0,"end":146},"obj":"Sentence"},{"id":"T93","span":{"begin":147,"end":540},"obj":"Sentence"},{"id":"T94","span":{"begin":541,"end":669},"obj":"Sentence"},{"id":"T95","span":{"begin":670,"end":895},"obj":"Sentence"},{"id":"T96","span":{"begin":896,"end":1189},"obj":"Sentence"},{"id":"T97","span":{"begin":1190,"end":1359},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"There are innumerable studies that have demonstrated that heparin can dampen inflammation through its interaction with key inflammatory mediators. The proinflammatory transcription factor nuclear factor-κB (NF-κB), which has been found to be involved in the pathogenesis of SARS-CoV, the virus underlying the 2003 severe acute respiratory syndrome (SARS) epidemic (16), leads to the production of downstream inflammatory cytokines and other immune response proteins including tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 (13, 47). Heparin has been observed to directly dampen NF-κB signaling in LPS-stimulated human endothelial cells and human monocytes (21). Similarly, a synthetic heparin-like drug has recently been developed that neutralizes high mobility group box 1 (HMGB1; 5), a proinflammatory mediator that is known to play a role in the pathogenesis of viral infections (15). With respect to inflammatory cell infiltration, a phenomenon that has been observed pathologically in COVID-19 (2, 39), heparin can directly interact with vascular endothelial cells leading to reduced recruitment of the innate immune system and direct inhibition of neutrophil activation (13). More broadly, heparin has been shown to dampen inflammation in other preclinical models characterized by robust inflammation including pancreatitis (12) and sepsis (33)."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T33","span":{"begin":476,"end":481},"obj":"Phenotype"},{"id":"T34","span":{"begin":1325,"end":1337},"obj":"Phenotype"},{"id":"T35","span":{"begin":1347,"end":1353},"obj":"Phenotype"}],"attributes":[{"id":"A33","pred":"hp_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/HP_0002664"},{"id":"A34","pred":"hp_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/HP_0001733"},{"id":"A35","pred":"hp_id","subj":"T35","obj":"http://purl.obolibrary.org/obo/HP_0100806"}],"text":"There are innumerable studies that have demonstrated that heparin can dampen inflammation through its interaction with key inflammatory mediators. The proinflammatory transcription factor nuclear factor-κB (NF-κB), which has been found to be involved in the pathogenesis of SARS-CoV, the virus underlying the 2003 severe acute respiratory syndrome (SARS) epidemic (16), leads to the production of downstream inflammatory cytokines and other immune response proteins including tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 (13, 47). Heparin has been observed to directly dampen NF-κB signaling in LPS-stimulated human endothelial cells and human monocytes (21). Similarly, a synthetic heparin-like drug has recently been developed that neutralizes high mobility group box 1 (HMGB1; 5), a proinflammatory mediator that is known to play a role in the pathogenesis of viral infections (15). With respect to inflammatory cell infiltration, a phenomenon that has been observed pathologically in COVID-19 (2, 39), heparin can directly interact with vascular endothelial cells leading to reduced recruitment of the innate immune system and direct inhibition of neutrophil activation (13). More broadly, heparin has been shown to dampen inflammation in other preclinical models characterized by robust inflammation including pancreatitis (12) and sepsis (33)."}

{"project":"2_test","denotations":[{"id":"32519894-17141229-2138187","span":{"begin":365,"end":367},"obj":"17141229"},{"id":"32519894-31030744-2138188","span":{"begin":532,"end":534},"obj":"31030744"},{"id":"32519894-17727922-2138189","span":{"begin":536,"end":538},"obj":"17727922"},{"id":"32519894-32063752-2138190","span":{"begin":665,"end":667},"obj":"32063752"},{"id":"32519894-32188725-2138191","span":{"begin":790,"end":791},"obj":"32188725"},{"id":"32519894-24717031-2138192","span":{"begin":891,"end":893},"obj":"24717031"},{"id":"32519894-32437596-2138193","span":{"begin":1008,"end":1009},"obj":"32437596"},{"id":"32519894-32325026-2138194","span":{"begin":1011,"end":1013},"obj":"32325026"},{"id":"32519894-31030744-2138195","span":{"begin":1185,"end":1187},"obj":"31030744"},{"id":"32519894-14739847-2138196","span":{"begin":1339,"end":1341},"obj":"14739847"},{"id":"32519894-22820644-2138197","span":{"begin":1355,"end":1357},"obj":"22820644"}],"text":"There are innumerable studies that have demonstrated that heparin can dampen inflammation through its interaction with key inflammatory mediators. The proinflammatory transcription factor nuclear factor-κB (NF-κB), which has been found to be involved in the pathogenesis of SARS-CoV, the virus underlying the 2003 severe acute respiratory syndrome (SARS) epidemic (16), leads to the production of downstream inflammatory cytokines and other immune response proteins including tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 (13, 47). Heparin has been observed to directly dampen NF-κB signaling in LPS-stimulated human endothelial cells and human monocytes (21). Similarly, a synthetic heparin-like drug has recently been developed that neutralizes high mobility group box 1 (HMGB1; 5), a proinflammatory mediator that is known to play a role in the pathogenesis of viral infections (15). With respect to inflammatory cell infiltration, a phenomenon that has been observed pathologically in COVID-19 (2, 39), heparin can directly interact with vascular endothelial cells leading to reduced recruitment of the innate immune system and direct inhibition of neutrophil activation (13). More broadly, heparin has been shown to dampen inflammation in other preclinical models characterized by robust inflammation including pancreatitis (12) and sepsis (33)."}