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1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. 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1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

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{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T43","span":{"begin":102,"end":108},"obj":"Disease"},{"id":"T44","span":{"begin":457,"end":492},"obj":"Disease"},{"id":"T45","span":{"begin":463,"end":492},"obj":"Disease"},{"id":"T46","span":{"begin":494,"end":498},"obj":"Disease"},{"id":"T47","span":{"begin":530,"end":577},"obj":"Disease"},{"id":"T48","span":{"begin":530,"end":563},"obj":"Disease"},{"id":"T49","span":{"begin":579,"end":587},"obj":"Disease"},{"id":"T50","span":{"begin":579,"end":583},"obj":"Disease"},{"id":"T51","span":{"begin":695,"end":704},"obj":"Disease"},{"id":"T52","span":{"begin":708,"end":716},"obj":"Disease"},{"id":"T53","span":{"begin":708,"end":712},"obj":"Disease"},{"id":"T54","span":{"begin":833,"end":850},"obj":"Disease"},{"id":"T56","span":{"begin":844,"end":850},"obj":"Disease"},{"id":"T57","span":{"begin":957,"end":965},"obj":"Disease"},{"id":"T58","span":{"begin":957,"end":961},"obj":"Disease"},{"id":"T59","span":{"begin":1019,"end":1038},"obj":"Disease"},{"id":"T60","span":{"begin":1029,"end":1038},"obj":"Disease"},{"id":"T61","span":{"begin":1100,"end":1124},"obj":"Disease"},{"id":"T62","span":{"begin":1126,"end":1134},"obj":"Disease"}],"attributes":[{"id":"A43","pred":"mondo_id","subj":"T43","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A44","pred":"mondo_id","subj":"T44","obj":"http://purl.obolibrary.org/obo/MONDO_0006502"},{"id":"A45","pred":"mondo_id","subj":"T45","obj":"http://purl.obolibrary.org/obo/MONDO_0009971"},{"id":"A46","pred":"mondo_id","subj":"T46","obj":"http://purl.obolibrary.org/obo/MONDO_0006502"},{"id":"A47","pred":"mondo_id","subj":"T47","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A48","pred":"mondo_id","subj":"T48","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A49","pred":"mondo_id","subj":"T49","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A50","pred":"mondo_id","subj":"T50","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A51","pred":"mondo_id","subj":"T51","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A52","pred":"mondo_id","subj":"T52","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A53","pred":"mondo_id","subj":"T53","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A54","pred":"mondo_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/MONDO_0006502"},{"id":"A55","pred":"mondo_id","subj":"T54","obj":"http://purl.obolibrary.org/obo/MONDO_0015796"},{"id":"A56","pred":"mondo_id","subj":"T56","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A57","pred":"mondo_id","subj":"T57","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A58","pred":"mondo_id","subj":"T58","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A59","pred":"mondo_id","subj":"T59","obj":"http://purl.obolibrary.org/obo/MONDO_0005812"},{"id":"A60","pred":"mondo_id","subj":"T60","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A61","pred":"mondo_id","subj":"T61","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A62","pred":"mondo_id","subj":"T62","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T57","span":{"begin":59,"end":74},"obj":"http://purl.obolibrary.org/obo/CL_0000499"},{"id":"T58","span":{"begin":97,"end":101},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T59","span":{"begin":97,"end":101},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T60","span":{"begin":347,"end":348},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T61","span":{"begin":363,"end":364},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T62","span":{"begin":514,"end":515},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T63","span":{"begin":601,"end":602},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T64","span":{"begin":603,"end":623},"obj":"http://purl.obolibrary.org/obo/CL_0000082"},{"id":"T65","span":{"begin":839,"end":843},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T66","span":{"begin":839,"end":843},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T67","span":{"begin":968,"end":972},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T68","span":{"begin":968,"end":972},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T69","span":{"begin":1078,"end":1082},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T70","span":{"begin":1384,"end":1386},"obj":"http://purl.obolibrary.org/obo/CLO_0002860"},{"id":"T71","span":{"begin":1393,"end":1405},"obj":"http://purl.obolibrary.org/obo/CL_0000312"},{"id":"T72","span":{"begin":1477,"end":1481},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T73","span":{"begin":1492,"end":1499},"obj":"http://purl.obolibrary.org/obo/PR_000009054"},{"id":"T74","span":{"begin":1583,"end":1586},"obj":"http://purl.obolibrary.org/obo/CLO_0003740"},{"id":"T75","span":{"begin":1614,"end":1622},"obj":"http://purl.obolibrary.org/obo/CL_0000623"},{"id":"T76","span":{"begin":1624,"end":1644},"obj":"http://purl.obolibrary.org/obo/CL_0000623"},{"id":"T77","span":{"begin":1674,"end":1679},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T78","span":{"begin":1688,"end":1693},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"}],"text":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T19","span":{"begin":1255,"end":1257},"obj":"Chemical"},{"id":"T21","span":{"begin":1272,"end":1275},"obj":"Chemical"},{"id":"T22","span":{"begin":1277,"end":1300},"obj":"Chemical"},{"id":"T23","span":{"begin":1286,"end":1292},"obj":"Chemical"},{"id":"T24","span":{"begin":1308,"end":1319},"obj":"Chemical"},{"id":"T25","span":{"begin":1364,"end":1368},"obj":"Chemical"},{"id":"T26","span":{"begin":1370,"end":1386},"obj":"Chemical"},{"id":"T28","span":{"begin":1370,"end":1383},"obj":"Chemical"},{"id":"T29","span":{"begin":1425,"end":1427},"obj":"Chemical"},{"id":"T30","span":{"begin":1429,"end":1431},"obj":"Chemical"},{"id":"T32","span":{"begin":1443,"end":1453},"obj":"Chemical"},{"id":"T33","span":{"begin":1492,"end":1499},"obj":"Chemical"},{"id":"T34","span":{"begin":1557,"end":1559},"obj":"Chemical"},{"id":"T36","span":{"begin":1652,"end":1662},"obj":"Chemical"}],"attributes":[{"id":"A19","pred":"chebi_id","subj":"T19","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A20","pred":"chebi_id","subj":"T19","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A21","pred":"chebi_id","subj":"T21","obj":"http://purl.obolibrary.org/obo/CHEBI_26523"},{"id":"A22","pred":"chebi_id","subj":"T22","obj":"http://purl.obolibrary.org/obo/CHEBI_26523"},{"id":"A23","pred":"chebi_id","subj":"T23","obj":"http://purl.obolibrary.org/obo/CHEBI_25805"},{"id":"A24","pred":"chebi_id","subj":"T24","obj":"http://purl.obolibrary.org/obo/CHEBI_48433"},{"id":"A25","pred":"chebi_id","subj":"T25","obj":"http://purl.obolibrary.org/obo/CHEBI_15551"},{"id":"A26","pred":"chebi_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/CHEBI_15551"},{"id":"A27","pred":"chebi_id","subj":"T26","obj":"http://purl.obolibrary.org/obo/CHEBI_606564"},{"id":"A28","pred":"chebi_id","subj":"T28","obj":"http://purl.obolibrary.org/obo/CHEBI_26333"},{"id":"A29","pred":"chebi_id","subj":"T29","obj":"http://purl.obolibrary.org/obo/CHEBI_33325"},{"id":"A30","pred":"chebi_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A31","pred":"chebi_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A32","pred":"chebi_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/CHEBI_48706"},{"id":"A33","pred":"chebi_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/CHEBI_145810"},{"id":"A34","pred":"chebi_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/CHEBI_34827"},{"id":"A35","pred":"chebi_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/CHEBI_51112"},{"id":"A36","pred":"chebi_id","subj":"T36","obj":"http://purl.obolibrary.org/obo/CHEBI_52999"}],"text":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T9","span":{"begin":500,"end":512},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T10","span":{"begin":641,"end":646},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T11","span":{"begin":1186,"end":1206},"obj":"http://purl.obolibrary.org/obo/GO_1905517"},{"id":"T12","span":{"begin":1238,"end":1246},"obj":"http://purl.obolibrary.org/obo/GO_0070265"},{"id":"T13","span":{"begin":1238,"end":1246},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T14","span":{"begin":1238,"end":1246},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T15","span":{"begin":1238,"end":1246},"obj":"http://purl.obolibrary.org/obo/GO_0001906"},{"id":"T16","span":{"begin":1406,"end":1412},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T17","span":{"begin":1421,"end":1427},"obj":"http://purl.obolibrary.org/obo/GO_0005152"},{"id":"T18","span":{"begin":1505,"end":1511},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T19","span":{"begin":1599,"end":1605},"obj":"http://purl.obolibrary.org/obo/GO_0040007"}],"text":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T10","span":{"begin":463,"end":483},"obj":"Phenotype"},{"id":"T11","span":{"begin":651,"end":665},"obj":"Phenotype"},{"id":"T12","span":{"begin":833,"end":850},"obj":"Phenotype"},{"id":"T13","span":{"begin":1231,"end":1237},"obj":"Phenotype"}],"attributes":[{"id":"A10","pred":"hp_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/HP_0002098"},{"id":"A11","pred":"hp_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/HP_0033041"},{"id":"A12","pred":"hp_id","subj":"T12","obj":"http://www.orpha.net/ORDO/Orphanet_178320"},{"id":"A13","pred":"hp_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/HP_0002664"}],"text":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

{"project":"MyTest","denotations":[{"id":"32265310-28306336-29390440","span":{"begin":885,"end":886},"obj":"28306336"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

{"project":"2_test","denotations":[{"id":"32265310-28306336-29390440","span":{"begin":885,"end":886},"obj":"28306336"}],"text":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

{"project":"LitCovid-sentences","denotations":[{"id":"T35","span":{"begin":0,"end":851},"obj":"Sentence"},{"id":"T36","span":{"begin":852,"end":1180},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}

{"project":"LitCovid-PubTator","denotations":[{"id":"263","span":{"begin":85,"end":108},"obj":"Disease"}],"attributes":[{"id":"A263","pred":"tao:has_database_id","subj":"263","obj":"MESH:D012131"}],"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":"FIGURE 1 Potential therapeutic effects of mesenchymal stem (stromal) cells (MSCs) in respiratory lung injury are mediated by different mechanisms, including but not limited to secreted paracrine factors, extracellular vesicles (EVs) and possibly mitochondrial transfer, promoting tissue protection, immunomodulation and possibly viral resistance. a) Schematic of a healthy alveolus (top) and inflamed/oedematous alveolus (bottom) and mechanisms involved in acute respiratory distress syndrome (ARDS) pathogenesis. b) Schematic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infecting a lung epithelial cell, with subsequent lysis and cytokine storm (left), and of potential MSC infection by SARS-CoV-2, with unknown downstream consequences (right). c) Some of the known mechanisms by which MSCs ameliorate non-viral acute lung injury. Adapted from Laffey and Matthay [9]. d) Limited information on mechanisms by which MSCs might ameliorate SARS-CoV-2 lung damage, based on limited pre-clinical data in influenza infection models. e) Current state-of-the-art of cell-based therapy in coronavirus disease 2019 (COVID-19), based on pre-clinical and clinical studies. MIF: macrophage migration inhibitory factor; TNF: tumour necrosis factor; IL: interleukin; ROS: reactive oxygen species; ACE2: angiotensin-converting enzyme 2; Ang-1: angiopoietin-1; PGE2: prostaglandin E2; KGF: keratinocyte growth factor; IL1-Ra: IL-1 receptor antagonist; TSG-6: TNF-stimulated gene 6; IGF-1: insulin-like growth factor 1; miRNAs: microRNAs; MΦ: macrophage; M2 MΦ: macrophage type 2; HGF: hepatocyte growth factor; NK cells: natural killer cells; ISGs: interferon-stimulated genes; hACE2: human ACE2."}