International immunopharmacology
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Int. Immunopharmacol. · Dec 2015
Protective effects of polydatin on lipopolysaccharide-induced acute lung injury through TLR4-MyD88-NF-κB pathway.
The purpose of this study was to investigate the protective effect of PD against lipopolysaccharide (LPS)-induced acute lung injury (ALI) and explore its potential mechanism. In vivo, PD and dexamethasone were intraperitoneally administered 1h before LPS stimulation. Then, mice were sacrificed at 6h post-LPS stimulation. ⋯ In vitro assays, PD effectively negatively mediated the inflammatory cytokines and ameliorated the high expressions of TLR4, MyD88, NF-κB caused by LPS simulation in Human bronchial epithelial BEAS-2B cells. This study indicated that PD played a protective role in LPS-induced ALI and BEAS-2B cells. The results supported further study of PD as potential candidate for acute lung injury.
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Int. Immunopharmacol. · Dec 2015
Ulinastatin inhibits the inflammation of LPS-induced acute lung injury in mice via regulation of AMPK/NF-κB pathway.
Ulinastatin (ULI), a serine protease inhibitor, had been widely used as a drug for patients with acute inflammatory disorders. However, evidence regarding the anti-inflammatory effect of ulinastatin was still lacking. In this study, we investigated the protective mechanisms of ULI in LPS-induced acute lung injury (ALI). ⋯ The results presented here indicated that ULI has a protective effect against LPS-induced ALI and this effect may be attributed partly to decreased production of proinflammatory cytokines through the regulation of AMPK/NF-κB signaling pathway.
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Int. Immunopharmacol. · Oct 2015
Hyaluronan ameliorates LPS-induced acute lung injury in mice via Toll-like receptor (TLR) 4-dependent signaling pathways.
Toll-like receptor-4 (TLR4) signaling has been implicated in innate immunity and acute inflammation following acute lung injury (ALI). As such, modulating inflammatory response through TLR4 represents an attractive therapeutic approach to treat ALI. Increasing evidence demonstrates that hyaluronan (HA) can modulate TLR4 activation and has shown early promise as a therapeutic agent in ALI. ⋯ Furthermore, we compared the protection effect of HA in TLR4-deficient mice with those of genetically matched wild type (WT) mice in an acute model of lung injury. However, in TLR4-deficient mice, HA pretreatment before LPS instillation fail to affect the LPS response. Therefore, our findings suggest that HA pretreatment attenuated LPS-induced ALI and the anti-inflammatory function of HA was partial dependent on TLR4, which shed new light on potential elements that regulate the lung injury response.
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Int. Immunopharmacol. · Sep 2015
Review Meta AnalysisEfficacy and safety of dendritic cells co-cultured with cytokine-induced killer cells immunotherapy for non-small-cell lung cancer.
Dendritic cells co-cultured with cytokine-induced killer cells (DC-CIK) immunotherapy has been widely studied and might be a new therapeutic strategy for non-small-cell lung cancer (NSCLC). We aimed to comprehensively and quantitatively evaluate the efficacy and safety of DC-CIK immunotherapy in NSCLC. Pubmed, Embase, Cochrane Library, and Web of Science were searched for randomized controlled trials comparing DC-CIK immunotherapy with control therapies in NSCLC. ⋯ The risks of all-grade anemia, leukopenia, dermatosis, diarrhea, nausea, acratia, and chest distress in patients receiving DC-CIK immunotherapy were comparable to those receiving control therapies. This meta-analysis demonstrates DC-CIK immunotherapy has superiority in PFS, OS, and DCR for NSCLC patients, and no more serious adverse events appeared. Further studies to provide solid evidence for the routine clinical use of DC-CIK immunotherapy are urgently needed.
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Hypoxia is an important factor for transcriptional regulation of cell metabolism and the adaptation to cellular stress. It modulates the function of phagocytic cells by stimulating surface receptors such as scavenger receptors, toll like receptors and their downstream signaling cascades. In response to hypoxia, innate immune modifiers are upregulated through pathways involving the key immune response master regulator nuclear factor-κB leading to the modulation of inflammatory cytokines. In this review, we highlighted the effects of hypoxia on different innate immune factors and consequences thereof.