Modulation of inflammatory and oxidative stress biomarkers due to dexamethasone exposure in chicken splenocytes

Abstract

Dexamethasone (DEXA) is a potent corticosteroid, commonly used for treating inflammatory, hypersensitive and allergic conditions. It is administered to birds with tumours. Many studies were conducted on its immunosuppressive effects; however none of the similar study is available employing chicken splenocytes culture system. The present study was conducted to assess DEXA induced alterations in inflammatory and oxidative stress biomarkers in chicken splenocytes due to its in vitro exposure. The maximum non-cytotoxic dose (MNCD) was evaluated and was further used for conducting lymphocytes proliferation assay (LPA), antioxidant assays (lipid peroxidation, GSH, superoxide dismutase and nitric oxide assays) and assessment of mRNA levels of various genes (IL-1β, IL-6, IL-10, LITAF, iNOS, NF-κB1, Nrf-2, Caspase-3 and -9) through qPCR. The MNCD was determined to be 30 ng/ml in chicken splenocytes culture system. DEXA caused reduction in B and T lymphocytes proliferation indicating its immunosuppressive effects, however improved the antioxidant status of the exposed splenocytes. The expression levels of IL-1β, IL-6, iNOS, LITAF and NF-κB1 were significantly reduced while IL-10 was enhanced, which signify potent anti-inflammatory potential of DEXA. NF-κB is a major transcription factor that regulates genes responsible for both, innate and adaptive immune responses and elicits inflammation. The nuclear factor erythroid 2-related factor 2 (Nrf-2) level was found to be up-regulated. Nrf-2 plays important role in combating the oxidant stress and its increased expression could be the reason of improved antioxidant status of DEXA exposed cells. Present findings indicated that DEXA exhibited modulation in anti-inflammatory, immunomodulatory and antioxidant mediators in chicken splenocytes.