PubMed:9317151
Annnotations
Inflammaging
{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":99},"obj":"Sentence"},{"id":"T2","span":{"begin":100,"end":215},"obj":"Sentence"},{"id":"T3","span":{"begin":216,"end":330},"obj":"Sentence"},{"id":"T4","span":{"begin":331,"end":590},"obj":"Sentence"},{"id":"T5","span":{"begin":591,"end":712},"obj":"Sentence"},{"id":"T6","span":{"begin":713,"end":961},"obj":"Sentence"},{"id":"T7","span":{"begin":962,"end":1125},"obj":"Sentence"},{"id":"T8","span":{"begin":1126,"end":1435},"obj":"Sentence"},{"id":"T9","span":{"begin":1436,"end":1641},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":99},"obj":"Sentence"},{"id":"T2","span":{"begin":100,"end":215},"obj":"Sentence"},{"id":"T3","span":{"begin":216,"end":330},"obj":"Sentence"},{"id":"T4","span":{"begin":331,"end":590},"obj":"Sentence"},{"id":"T5","span":{"begin":591,"end":712},"obj":"Sentence"},{"id":"T6","span":{"begin":713,"end":961},"obj":"Sentence"},{"id":"T7","span":{"begin":962,"end":1125},"obj":"Sentence"},{"id":"T8","span":{"begin":1126,"end":1435},"obj":"Sentence"},{"id":"T9","span":{"begin":1436,"end":1641},"obj":"Sentence"}],"text":"Dual effects of LPS antibodies on cellular uptake of LPS and LPS-induced proinflammatory functions.\nHuman phagocytes recognize bacterial LPS (endotoxin) through membrane CD14 (mCD14), a proinflammatory LPS receptor. This study tested the hypothesis that anti-LPS Abs neutralize endotoxin by blocking cellular uptake through mCD14. Ab-associated changes in the uptake and cellular distribution of FITC-LPS were assessed by flow cytometry and laser scanning confocal microscopy in human CD14-transfected Chinese hamster ovary fibroblasts (CHO-CD14 cells) and human peripheral blood monocytes. LPS core- and O-side chain-specific mAbs inhibited mCD14-mediated LPS uptake by both cell types in the presence of serum. O-side chain-specific mAb concurrently enhanced complement-dependent LPS uptake by monocytes through complement receptor-1 (CR1) and uptake by CHO-CD14 cells involving another heat-labile serum factor(s) and cell-associated recognition molecule(s). Core-specific mAb inhibited mCD14-mediated uptake of homologous and heterologous LPS, while producing less concurrent enhancement of non-mCD14-mediated LPS uptake. The modulation by anti-LPS mAbs of mCD14-mediated LPS uptake was associated with inhibition of LPS-induced nuclear factor-kappaB (NF-kappaB) translocation and TNF-alpha secretion in CHO-CD14 cells and monocytes, respectively, while mAb enhancement of non-mCD14-mediated LPS uptake stimulated these activities. LPS-specific Abs thus mediate anti-inflammatory and proinflammatory functions, respectively, by preventing target cell uptake of LPS through mCD14 and augmenting uptake through CR1 or other cell receptors."}
jnlpba-st-training
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pubmed-sentences-benchmark
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genia-medco-coref
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GENIAcorpus
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This study tested the hypothesis that anti-LPS Abs neutralize endotoxin by blocking cellular uptake through mCD14. Ab-associated changes in the uptake and cellular distribution of FITC-LPS were assessed by flow cytometry and laser scanning confocal microscopy in human CD14-transfected Chinese hamster ovary fibroblasts (CHO-CD14 cells) and human peripheral blood monocytes. LPS core- and O-side chain-specific mAbs inhibited mCD14-mediated LPS uptake by both cell types in the presence of serum. O-side chain-specific mAb concurrently enhanced complement-dependent LPS uptake by monocytes through complement receptor-1 (CR1) and uptake by CHO-CD14 cells involving another heat-labile serum factor(s) and cell-associated recognition molecule(s). Core-specific mAb inhibited mCD14-mediated uptake of homologous and heterologous LPS, while producing less concurrent enhancement of non-mCD14-mediated LPS uptake. The modulation by anti-LPS mAbs of mCD14-mediated LPS uptake was associated with inhibition of LPS-induced nuclear factor-kappaB (NF-kappaB) translocation and TNF-alpha secretion in CHO-CD14 cells and monocytes, respectively, while mAb enhancement of non-mCD14-mediated LPS uptake stimulated these activities. LPS-specific Abs thus mediate anti-inflammatory and proinflammatory functions, respectively, by preventing target cell uptake of LPS through mCD14 and augmenting uptake through CR1 or other cell receptors."}