International immunopharmacology
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Int. Immunopharmacol. · Nov 2020
Randomized Controlled TrialInterferon β-1b in treatment of severe COVID-19: A randomized clinical trial.
In this study, efficacy and safety of interferon (IFN) β-1b in the treatment of patients with severe COVID-19 were evaluated. Among an open-label, randomized clinical trial, adult patients (≥18 years old) with severe COVID-19 were randomly assigned (1:1) to the IFN group or the control group. Patients in the IFN group received IFN β-1b (250 mcg subcutaneously every other day for two consecutive weeks) along with the national protocol medications while in the control group, patients received only the national protocol medications (lopinavir/ritonavir or atazanavir/ritonavir plus hydroxychloroquine for 7-10 days). ⋯ IFN β-1b was effective in shortening the time to clinical improvement without serious adverse events in patients with severe COVID-19. Furthermore, admission in ICU and need for invasive mechanical ventilation decreased following administration of IFN β-1b. Although 28-day mortality was lower in the IFN group, further randomized clinical trials with large sample size are needed for exact estimation of survival benefit of IFN β-1b.
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Int. Immunopharmacol. · Nov 2020
Chebulanin exerts its anti-inflammatory and anti-arthritic effects via inhibiting NF-κB and MAPK activation in collagen-induced arthritis mice.
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by synovial inflammation and progressive joint destruction. Chebulanin is a natural polyphenol acid isolated from the traditional Tibetan medicine Terminalia chebula Retz that has previously been reported to possess anti-inflammatory properties. The present study aimed to investigate the anti-inflammatory and anti-arthritic effects of chebulanin and explore its underlying mechanisms in vivo and in vitro using a collagen-induced arthritis (CIA) mouse model and lipopolysaccharide (LPS) stimulated RAW264.7 cell inflammation model. ⋯ Furthermore, chebulanin reduced the levels of excised phosphorylated (p)-p38, phosphorylated-c-JUN N-terminal kinase (p-JNK), p-p65 and phosphorylated NF-κB inhibitor alpha (p-IκBα) in CIA mice, but did not affect the level of phosphorylated extracellular-signal-regulated kinase (ERK). In addition, chebulanin could inhibit the nuclear translocation of p38 and p65 in LPS-stimulated macrophages in dose-dependent manner. In conclusion, this study demonstrated that chebulanin exerts anti-inflammatory and anti-arthritic effects by inhibiting the activation of NF-κB and MAPK signaling pathways.
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Int. Immunopharmacol. · Nov 2020
LncRNA-5657 silencing alleviates sepsis-induced lung injury by suppressing the expression of spinster homology protein 2.
LncRNAs are closely associated with many human major diseases, however, the roles of lncRNAs in sepsis-induced lung injury remain unclear. ⋯ LncRNA-5657 is closely associated with sepsis-induce lung injury. In vitro and in vivo data demonstrated that LncRNA-5657 silencing alleviates sepsis-induced lung injury by inhibiting lung inflammatory response via suppressing spns2 expression.
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Int. Immunopharmacol. · Oct 2020
Meta AnalysisDifferential risks of immune-related colitis among various immune checkpoint inhibitor regimens.
Colitis is a life-threatening and common immune-related adverse event in patients receiving immune checkpoint inhibitors (ICIs). Therefore, we performed a meta-analysis to assess the risk of immune-related colitis among various ICI treatment regimens. ⋯ Our meta-analysis indicates that CTLA-4 inhibitor is associated with a higher risk of colitis compared with PD-1/PD-L1 inhibitor, whether used as a monotherapy or combination immunotherapy. Importantly, the combination of PD-1/PD-L1 inhibitor with chemotherapy or targeted therapy may not increase the risk of colitis significantly compared to PD-1/PD-L1 inhibitor alone.
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Int. Immunopharmacol. · Oct 2020
Vildagliptin, a CD26/DPP4 inhibitor, ameliorates bleomycin-induced pulmonary fibrosis via regulating the extracellular matrix.
Idiopathic pulmonary fibrosis is a debilitating lung disease. CD26/DPP4 plays promotive roles in pulmonary damage and fibrosis. This study aimed to explore the roles of vildagliptin in bleomycin-induced pulmonary fibrosis, and to address its ameliorative effect on the extracellular matrix (ECM). ⋯ As an inhibitor of CD26/DPP4, Vildagliptin could be a promising therapeutic candidate for idiopathic pulmonary fibrosis.