Melioidosis, caused by Burkholderia pseudomallei is associated with high mortality due to overwhelming inflammatory response leading to septicaemia. Glycogen synthase kinase-3β (GSK3β) plays a central role in the regulation of pathogen-induced inflammatory response through modulation of pro- and anti-inflammatory cytokine production. Previous findings from our laboratory demonstrated that treatment with LiCL, a GSK3 inhibitor modulated the cytokine balance in B. pseudomallei-infected mice and increased animal survivability. Another inorganic salt, sodium tungstate (Na2WO4) which can induce ERK activation and trigger GSK3β phosphorylation also regulates the expression and secretion of pro- and anti- inflammatory cytokines. Here we extend our study to evaluate effects of Na2WO4 administration on the cytokine response towards B. pseudomallei infection in mice to reiterate involvement of GSK3β inhibition in modulating cytokine production in melioidosis. Pre- treatment with 100 mg/kg body weight Na2WO4 improved survivability (33.3 %) of B. pseudomallei-challenged mice (p<0.05). However, bacterial counts in liver and spleen of na2wo4-treated mice were not significantly different from that in non-treated controls. NA2WO4 administration resulted in increased phosphorylation of GSK3β in both liver and spleen samples by 2.2 and 3.3 fold respectively (p<0.05) compared to controls. Levels of pro-inflammatory cytokines, TNF-α and IFN-γ in sera of infected animals administered with Na2WO4 decreased by 15% whilst, the levels of anti-inflammatory cytokine, il-10 was elevated by 45% (p<0.05). Overall, the present findings reiterate our notion that inhibition of GSK3β, at least in part modulated the production of inflammatory cytokines induced during B. pseudomallei infection thus conferring survival advantage in infected animals tested.