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Heat shock up‐regulates expression of Toll‐like receptor‐2 and Toll‐like receptor‐4 in human monocytes via p38 kinase signal pathway

Heat stress can alert innate immunity by inducing stress proteins such as heat‐shock proteins (HSPs). However, it remains unclear whether heat stress affects the activation of antigen‐presenting cell (APC) in response to pathogen‐associated molecule patterns (PAMPs) by directly regulating pathogen recognition receptors (PRRs). As an important kind of PRRs, Toll‐like receptors (TLRs) play critical roles in the activation of immune system. In this study, we demonstrated that heat shock up‐regulated the expression of HSP70 as well as TLR2 and TLR4 in monocytes. The induction of TLRs was prior to that of HSP70, which suggesting the up‐regulation of TLR2 and TLR4 might be independent of the induction of HSP70. Heat shock activated p38 kinase, extracellular signal‐related kinase (ERK) and nuclear factor‐kappa B (NF‐κB) signal pathways in monocytes. Pretreatment with specific inhibitor of p38 kinase, but not those of ERK and NF‐κB, inhibited heat shock‐induced up‐regulation of TLR2 and TLR4. This indicates that p38 pathway takes part in heat shock‐induced up‐regulation of TLR2 and TLR4. Heat shock also increased lipoteichoic acid‐ or lipopolysaccharide‐induced interleukin‐6 production by monocytes. These results suggest that the p38 kinase‐mediated up‐regulation of TLR2 and TLR4 might be involved in the enhanced response to PAMP in human monocytes induced by heat shock.