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Nickel (Ni) ions easily elute from many alloys and elicit inflammation and allergies. Previous studies have shown that infections due to the implantation of medical devices cause inflammation and enhance the elution of Ni ions (Ni 2+ ). However, cross-talk between infection- and Ni 2+ -induced signaling pathways has not yet been elucidated in detail. In the present study, we investigated the effects of Ni 2+  on the lipopolysaccharide (LPS)-induced production of cytokines in a LPS-induced air pouch-type inflammation model in BALB/c mice and the murine macrophage cell line RAW264. We demonstrated that Ni 2+  inhibited the LPS-induced production of interleukin (IL)-6, but not that of tumor necrosis factor (TNF)-α both  in vivo  and  in vitro . This inhibitory effect was also observed with cobalt ion (Co 2+ ), but not with chloride ion (Cl - ), zinc ion (Zn 2+ ), or palladium ion (Pd 2+ ), and was highly selective to the production of IL-6. Ni 2+  did not inhibit the activation of ERK1/2, p38 MAPK, or JNK. Although Ni 2+  decreased IL-6 mRNA levels, it failed to inhibit the LPS-induced activation of the IL-6 promoter. An experiment using actinomycin D, a transcription inhibitor, revealed that Ni 2+  decreased the stability of IL-6 mRNA. Moreover, Ni 2+  inhibited the LPS-induced expression of Arid5a, but not regnase-1. These results demonstrated that Ni 2+  may have selectively inhibited the LPS-induced production of IL-6 by decreasing the Arid5a-dependent stabilization of IL-6 mRNA.

Nickel Ions Selectively Inhibit Lipopolysaccharide-Induced Interleukin-6 Production by Decreasing Its mRNA Stability