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pmc-enju-pas

bionlp-st-ge-2016-spacy-parsed

GO-BP

GO-MF

{"project":"GO-MF","denotations":[{"id":"T1003","span":{"begin":108,"end":115},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T1004","span":{"begin":143,"end":158},"obj":"http://purl.obolibrary.org/obo/GO_0042608"},{"id":"T1005","span":{"begin":264,"end":268},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T1006","span":{"begin":477,"end":481},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T1007","span":{"begin":910,"end":914},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T1008","span":{"begin":1848,"end":1852},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T1009","span":{"begin":2031,"end":2035},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T1010","span":{"begin":2151,"end":2155},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T1011","span":{"begin":901,"end":905},"obj":"http://purl.obolibrary.org/obo/GO_0005134"},{"id":"T1012","span":{"begin":1016,"end":1021},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T1013","span":{"begin":1445,"end":1454},"obj":"http://purl.obolibrary.org/obo/GO_0022809"},{"id":"T1014","span":{"begin":1622,"end":1625},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T1015","span":{"begin":1652,"end":1655},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T1016","span":{"begin":2042,"end":2045},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T1017","span":{"begin":1991,"end":1994},"obj":"http://purl.obolibrary.org/obo/GO_0004705"}],"text":"Background\nActivator protein (AP)-1 and nuclear factor (NF)-κB largely control T-cell activation, following binding of foreign antigens to the T-cell receptor leading to cytokine secretion. Elevated levels of pro-inflammatory cytokines and chemokines such as TNF, IL-6 and CXCL8 are associated with several human diseases including cystic fibrosis, pulmonary fibrosis and AIDS. The aim of this study was to investigate the role of the transcription factors, AP-1 and NF-κB, in IL-6 and CXCL8 regulation in Jurkat T-cells.\n\nResults\nPhorbol myristate acetate (PMA) exposure resulted in an up-regulation of AP-1 and down-regulation of NF-κB activity, however, exposure to heat killed (HK) Escherichia. coli MG1655 resulted in a dose-dependent increase in NF-κB activity without affecting AP-1. The cytokine profile revealed an up-regulation of the chemokine CXCL8 and the pro-inflammatory cytokines TNF, IL-2 and IL-6 following treatment with both PMA and HK E. coli, while the levels of the anti-inflammatory cytokine IL-10 were not affected by PMA but were significantly down-regulated by HK E. coli. AP-1 activation was significantly increased 2 h after PMA exposure and continued to increase thereafter. In contrast, NF-κB responded to PMA exposure by a rapid up-regulation followed by a subsequent down-regulation. Increased intracellular Ca2+ concentrations countered the down-regulation of NF-κB by PMA, while similar treatment with calcium ionophore resulted in a reduced NF-κB activity following induction with HK E. coli. In order to further study NF-κB activation, we considered two up-stream signalling proteins, PKC and Bcl10. Phosphorylated-PKC levels increased in response to PMA and HK E. coli, while Bcl10 levels significantly decreased following PMA treatment. Using an NF-κB activation inhibitor, we observed complete inhibition of IL-6 expression while CXCL8 levels only decreased by 40% at the highest concentration. Treatment of Jurkat T-cells with PMA in the presence of JNK-inhibitor suppressed both CXCL8 and IL-6 while PKC-inhibitor primarily decreased CXCL8 expression.\n\nConclusion\nThe present study shows that NF-κB regulated IL-6 but not CXCL8. This complex regulation of CXCL8 suggests that there is a need to further evaluate the signalling pathways in order to develop new treatment for diseases with elevated CXCL8 levels, such as AIDS and autoimmune diseases. "}

GO-CC

{"project":"GO-CC","denotations":[{"id":"T1019","span":{"begin":515,"end":520},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T1020","span":{"begin":1957,"end":1962},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T1021","span":{"begin":143,"end":158},"obj":"http://purl.obolibrary.org/obo/GO_0042101"},{"id":"T1022","span":{"begin":1327,"end":1340},"obj":"http://purl.obolibrary.org/obo/GO_0005622"}],"text":"Background\nActivator protein (AP)-1 and nuclear factor (NF)-κB largely control T-cell activation, following binding of foreign antigens to the T-cell receptor leading to cytokine secretion. Elevated levels of pro-inflammatory cytokines and chemokines such as TNF, IL-6 and CXCL8 are associated with several human diseases including cystic fibrosis, pulmonary fibrosis and AIDS. The aim of this study was to investigate the role of the transcription factors, AP-1 and NF-κB, in IL-6 and CXCL8 regulation in Jurkat T-cells.\n\nResults\nPhorbol myristate acetate (PMA) exposure resulted in an up-regulation of AP-1 and down-regulation of NF-κB activity, however, exposure to heat killed (HK) Escherichia. coli MG1655 resulted in a dose-dependent increase in NF-κB activity without affecting AP-1. The cytokine profile revealed an up-regulation of the chemokine CXCL8 and the pro-inflammatory cytokines TNF, IL-2 and IL-6 following treatment with both PMA and HK E. coli, while the levels of the anti-inflammatory cytokine IL-10 were not affected by PMA but were significantly down-regulated by HK E. coli. AP-1 activation was significantly increased 2 h after PMA exposure and continued to increase thereafter. In contrast, NF-κB responded to PMA exposure by a rapid up-regulation followed by a subsequent down-regulation. Increased intracellular Ca2+ concentrations countered the down-regulation of NF-κB by PMA, while similar treatment with calcium ionophore resulted in a reduced NF-κB activity following induction with HK E. coli. In order to further study NF-κB activation, we considered two up-stream signalling proteins, PKC and Bcl10. Phosphorylated-PKC levels increased in response to PMA and HK E. coli, while Bcl10 levels significantly decreased following PMA treatment. Using an NF-κB activation inhibitor, we observed complete inhibition of IL-6 expression while CXCL8 levels only decreased by 40% at the highest concentration. Treatment of Jurkat T-cells with PMA in the presence of JNK-inhibitor suppressed both CXCL8 and IL-6 while PKC-inhibitor primarily decreased CXCL8 expression.\n\nConclusion\nThe present study shows that NF-κB regulated IL-6 but not CXCL8. This complex regulation of CXCL8 suggests that there is a need to further evaluate the signalling pathways in order to develop new treatment for diseases with elevated CXCL8 levels, such as AIDS and autoimmune diseases. "}

sentences

ICD10

{"project":"ICD10","denotations":[{"id":"T1002","span":{"begin":332,"end":358},"obj":"http://purl.bioontology.org/ontology/ICD10/E84.0"},{"id":"T1000","span":{"begin":332,"end":347},"obj":"http://purl.bioontology.org/ontology/ICD10/E84"},{"id":"T1001","span":{"begin":332,"end":347},"obj":"http://purl.bioontology.org/ontology/ICD10/E84.9"}],"text":"Background\nActivator protein (AP)-1 and nuclear factor (NF)-κB largely control T-cell activation, following binding of foreign antigens to the T-cell receptor leading to cytokine secretion. Elevated levels of pro-inflammatory cytokines and chemokines such as TNF, IL-6 and CXCL8 are associated with several human diseases including cystic fibrosis, pulmonary fibrosis and AIDS. The aim of this study was to investigate the role of the transcription factors, AP-1 and NF-κB, in IL-6 and CXCL8 regulation in Jurkat T-cells.\n\nResults\nPhorbol myristate acetate (PMA) exposure resulted in an up-regulation of AP-1 and down-regulation of NF-κB activity, however, exposure to heat killed (HK) Escherichia. coli MG1655 resulted in a dose-dependent increase in NF-κB activity without affecting AP-1. The cytokine profile revealed an up-regulation of the chemokine CXCL8 and the pro-inflammatory cytokines TNF, IL-2 and IL-6 following treatment with both PMA and HK E. coli, while the levels of the anti-inflammatory cytokine IL-10 were not affected by PMA but were significantly down-regulated by HK E. coli. AP-1 activation was significantly increased 2 h after PMA exposure and continued to increase thereafter. In contrast, NF-κB responded to PMA exposure by a rapid up-regulation followed by a subsequent down-regulation. Increased intracellular Ca2+ concentrations countered the down-regulation of NF-κB by PMA, while similar treatment with calcium ionophore resulted in a reduced NF-κB activity following induction with HK E. coli. In order to further study NF-κB activation, we considered two up-stream signalling proteins, PKC and Bcl10. Phosphorylated-PKC levels increased in response to PMA and HK E. coli, while Bcl10 levels significantly decreased following PMA treatment. Using an NF-κB activation inhibitor, we observed complete inhibition of IL-6 expression while CXCL8 levels only decreased by 40% at the highest concentration. Treatment of Jurkat T-cells with PMA in the presence of JNK-inhibitor suppressed both CXCL8 and IL-6 while PKC-inhibitor primarily decreased CXCL8 expression.\n\nConclusion\nThe present study shows that NF-κB regulated IL-6 but not CXCL8. This complex regulation of CXCL8 suggests that there is a need to further evaluate the signalling pathways in order to develop new treatment for diseases with elevated CXCL8 levels, such as AIDS and autoimmune diseases. "}

events-check-again

bionlp-st-ge-2016-reference-tees

bionlp-st-ge-2016-reference

bionlp-st-ge-2016-uniprot

test2

PMC:2889865 / 80-2471 JSONTXT

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PMC:2889865 / 80-2471 JSON TXT