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Cobalt(II) Chloride Modifies the Phenotype of Macrophage Activation #MMPMID28244246
Kumanto M; Paukkeri EL; Nieminen R; Moilanen E
Basic Clin Pharmacol Toxicol 2017[Aug]; 121 (2): 98-105 PMID28244246show ga
Cobalt (Co) is vital for cells in trace amounts, but excessive exposure to Co is possible due to surgical devices such as artificial metal-on-metal joints. Cobalt(II) chloride (CoCl(2) ) has also been shown to imitate hypoxic conditions in cells by stabilizing the transcription factor hypoxia-inducible factor-1alpha (HIF-1alpha). The purpose of this study was to investigate the possible immunomodulatory action of CoCl(2) by investigating its effects on the expression of inflammatory genes in macrophages. The following factors were assessed: inducible nitric oxidase synthase (iNOS), nicotinamide adenine dinucleotide phosphate-oxidase 2 (NOX2), interleukin-6 (IL-6), arginase-1 and HIF-1alpha. In the absence of exogenous cytokines, CoCl(2) enhanced alternative (M2) macrophage activation as demonstrated by increased arginase-1 expression, but had no direct effect on inflammatory factors associated with classical (M1) activation. Interestingly, in lipopolysaccharide (LPS)-stimulated macrophages, CoCl(2) modified the M1-type activation profile by increasing iNOS expression and nitric oxide production and decreasing NOX2 and IL-6. Also, CoCl(2) increased HIF-1alpha levels in unstimulated and LPS-stimulated cells as expected. In conclusion, we showed that CoCl(2) enhanced alternative (M2) activation in resting macrophages. In addition, CoCl(2) was found to remodel the classical M1 phenotype of macrophage activation by changing the balance of iNOS, NOX2 and IL-6.
Basic+Clin+Pharmacol+Toxicol 2017 ; 121 (2): 98-105
