International immunopharmacology
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Int. Immunopharmacol. · Dec 2015
GTS-21 attenuates lipopolysaccharide-induced inflammatory cytokine production in vitro by modulating the Akt and NF-κB signaling pathway through the α7 nicotinic acetylcholine receptor.
GTS-21, a selective α7 nicotinic acetylcholine receptor agonist, has recently been established as a promising treatment for inflammation. However, the detailed molecular mechanism of GTS-21 in suppressing pro-inflammatory cytokine production is only partially explored. The study aimed to analyze cytokine expression suppressed by GTS-21 with lipopolysaccharide (LPS)-induced inflammation in vitro and to gain insights into the role of Akt/NF-κB signaling pathway in this process. ⋯ These findings indicate that GTS-21 suppresses LPS-induced inflammation by inhibiting the Akt/NF-κB signal pathway through α7 nAChR. GTS-21 has a potential application in inflammatory disease therapy.
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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
Intranasal administration of CpG oligodeoxynucleotides reduces lower airway inflammation in a murine model of combined allergic rhinitis and asthma syndrome.
Given the relationship between allergic rhinitis (AR) and asthma, it can be hypothesized that reducing upper airway inflammation by targeting oligodeoxynucleotides with CpG motifs (CpG-ODN) specifically to the upper airway via intranasal administration in a small volume (10 μL) might improve lower airway (asthma) outcomes. The goal of this study was to investigate the therapeutic efficacy of 10 μL of intranasal versus intradermal administration of CpG-ODN in suppressing lower airway inflammation and methacholine-induced airway hyperreactivity (AHR) in mice subjected to ovalbumin (OVA)-induced combined allergic rhinitis and asthma syndrome (CARAS). OVA-sensitized BALB/c mice were subjected to upper-airway intranasal OVA exposure three times per week for 3 weeks. ⋯ In conclusion, intranasal treatment with CpG-ODN attenuated AR and significantly alleviated lower airway inflammation and AHR in the CARAS model. CpG-ODN therapy was more effective when administered intranasally than when administered intradermally. The current study supports the development of CpG-ODN nasal spray as a novel therapeutic agent for CARAS.
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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.