| Summary: | The effects of Cobalt (II) chloride (CoCl<sub>2</sub>) in the context of <i>Brucella abortus</i> (<i>B. abortus</i>) infection have not been evaluated so far. Firstly, we found that CoCl<sub>2</sub> treatment inhibited the phagocytosis of <i>B. abortus</i> 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 <i>LAMP1</i>, <i>LAMP2</i>, and lysosomal enzyme <i>GLA</i> at the transcriptional level activated immune responses, weakening the <i>B. abortus</i> growth at 4 h post-infection (pi). The silencing of HIF-1α increased bacterial survival at 24 h pi. At the same time, CoCl<sub>2</sub> treatment showed a significant increase in the transcripts of lysosomal enzyme <i>HEXB</i> and cytokine <i>TNF-α</i> and an attenuation of the bacterial survival. Moreover, the enhancement at the protein level of HIF-1α was induced in the CoCl<sub>2</sub> treatment at both 4 and 24 h pi. Finally, our results demonstrated that CoCl<sub>2</sub> administration induced the production of serum cytokines IFN-γ and IL-6, which is accompanied by dampened <i>Brucella</i> proliferation in the spleen and liver of treated mice, and reduced the splenomegaly and hepatomegaly. Altogether, CoCl<sub>2</sub> treatment contributed to host resistance against <i>B. abortus</i> infection with immunomodulatory effects.
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