Abstract
Interleukin-6 (IL-6) is a pleiotropic cytokine involved in the regulation of the immune response and inflammation. In this study, we investigated effect of the proinflammatory cytokine interleukin-1β (IL-1β) on IL-6 expression in canine dermal fibroblasts. IL-1β induced IL-6 mRNA expression and protein release in a time- and dose-dependent manner. When cells were treated with inhibitors of mitogen-activated protein kinases (MAPKs), the extracellular signal-regulated kinase (ERK) inhibitor FR180240 inhibited IL-1β-induced IL-6 mRNA expression, but not SP600125 or SKF86002, which are c-Jun N-terminal kinase (JNK) and p38 MAPK inhibitors, respectively. In cells treated with U0126, an inhibitor of MAPK/ERK kinase (MEK), which activates ERK, IL-1β-induced IL-6 mRNA expression was also inhibited. IL-1β stimulated ERK1/2 phosphorylation. In cells transfected with ERK1 and ERK2 isoform siRNAs, IL-1β-induced IL-6 mRNA expression was reduced. These observations suggest that IL-1β induces IL-6 expression via ERK1/2 signaling pathway in canine dermal fibroblasts.
Highlights
Interleukin-6 (IL-6) is a pleiotropic cytokine involved in the regulation of the immune response and inflammation
After treatment with 100 pM IL-1β, a significant increase in IL-6 mRNA expression significantly increased at 3 h, reached a peak level at 6 h, and returned to the sustained levels that were slightly higher than the control (Fig 1C)
To confirm the compensation of ERK1 and ERK2 pathways, we examined the effect of IL-1β on IL-6 mRNA expression in the cells co-transfected with both ERK1 and ERK2 siRNAs
Summary
Interleukin-6 (IL-6) is a pleiotropic cytokine involved in the regulation of the immune response and inflammation. IL-6 is narrowly detectable in serum under physiological conditions, but its concentration dramatically increases during early phases of inflammation [1, 2]. In dogs with inflammation experimentally induced by an injection of turpentine oil [3] or canine sepsis models produced by administering infusions of either live Escherichia coli [4] or lipopolysaccharide (LPS) [5,6,7], induction of high levels of serum IL-6 are observed.
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