Cobalt (II) Chloride Regulates the Invasion and Survival of 544 in RAW 264.7 Cells and B6 Mice.

The effects of Cobalt (II) chloride (CoCl) in the context of () infection have not been evaluated so far. Firstly, we found that CoCl treatment inhibited the phagocytosis of into RAW 264.7 cells. The inhibition of bacterial invasion was regulated by F-actin formation and associated with a reduction in the phosphorylation of ERK1/2 and HIF-1α expression. Secondly, the activation of trafficking regulators , , and lysosomal enzyme at the transcriptional level activated immune responses, weakening the growth at 4 h post-infection (pi). The silencing of HIF-1α increased bacterial survival at 24 h pi. At the same time, CoCl treatment showed a significant increase in the transcripts of lysosomal enzyme and cytokine and an attenuation of the bacterial survival. Moreover, the enhancement at the protein level of HIF-1α was induced in the CoCl treatment at both 4 and 24 h pi. Finally, our results demonstrated that CoCl administration induced the production of serum cytokines IFN-γ and IL-6, which is accompanied by dampened proliferation in the spleen and liver of treated mice, and reduced the splenomegaly and hepatomegaly. Altogether, CoCl treatment contributed to host resistance against infection with immunomodulatory effects.