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Esent study clearly demonstrated that LPS, as a TLR-4 agonist, but
In terms of the interaction between IL-32 and TLR-2/NOD2 (nucleotide-binding Theophylline biological activity oligomerization domain-containing protein 2) signaling, IL-32 has been reported to stimulate TNFa, IL-6, and IL-8 production by directly increasing expression of TLR-2 and NOD2 [32]. Conversely, the interaction of IL-32 with TLR-Nakayama et al. Arthritis Research Therapy 2012, 14:R120 http://arthritis-research.com/content/14/3/RPage 8 ofACBFigure 5 Exogenous `IL-32a induced‘ TNFa production by RAW 264.7 cells through activation of NF-B and ERK1/2 MAPK. Two different concentrations of rIL-32a or LPS were added to RAW 264.7 cells in culture, followed by incubation for 24 hours. The level of TNFa in culture media was measured by a specific enzyme-linked immunosorbent assay (a). IL-32a alone as PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28154141 well as LPS was capable of inducing TNFa secretion into culture media by RAW 264.7 cells. Conversely, the interaction of IL-32 with TLR-Nakayama et al. Arthritis Research Therapy 2012, 14:R120 http://arthritis-research.com/content/14/3/RPage 8 ofACBFigure 5 Exogenous `IL-32a induced‘ TNFa production by RAW 264.7 cells through activation of NF-B and ERK1/2 MAPK. Two different concentrations of rIL-32a or LPS were added to RAW 264.7 cells in culture, followed by incubation for 24 hours. The level of TNFa in culture media was measured by a specific enzyme-linked immunosorbent assay (a). IL-32a alone as PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28154141 well as LPS was capable of inducing TNFa secretion into culture media by RAW 264.7 cells. Values are expressed as ?standard deviation (SD) of four determinations. RAW 264.7 cells were cultured with or without rIL-32a for 24 hours in combination with inhibitors for IB and MAPKs, including DHMEQ, U0126, SB203580, and SP600125 (b). IL-32a-induced TNFa production was inhibited by DHMEQ or U0126 but not by SB203580 or SP600125 (*P < 0.05, **P < 0.01). Values are expressed as ?SD of four determinations. Phosphorylations of IB and MAPKs in RAW 264.7 cells were determined by Western blotting by using anti-phospho-IB, -ERK1/2, -p38, or -JNK antibodies after treatment with rIL-32a (100 ng/mL) (c). rIL-32a stimulated phosphorylation of IB and ERK1/2, starting at 30 minutes and peaking at 90 (ERK1/2) or 120 (IB) minutes, whereas significant phosphorylation was not observed in p38 or JNK. Degradation of IB was also observed with a peak at 90 minutes. These data represent one of three independent experiments. DHMEQ, dehydroxymethylepoxyquinomicin; DMSO, dimethyl sulfoxide; IB, inhibitor kappa B; IL, interleukin; LPS, lipopolysaccharide; MAPK, mitogen-activated protein kinase; NF-B, nuclear factor kappa B; rIL-32a, recombinant human interleukin-32a protein; TNFa, tumor necrosis factor-alpha.can be speculated to involve the binding of IL-32 to its putative receptor modulates downstream signaling for TLR-4 or other TLRs, since the proinflammatory activities of IL-32 were present even in macrophages derived from TLR-4 -/- mice, and stimulation with IL-32 plus TLR ligand elicited only additive effects rather than synergistic effects [33]. Two candidate molecules potentially connecting IL-32a and TLR-4 signaling are considered.
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