Ascorbic acid modulates cell migration in differentiated HL-60 cells and peripheral blood leukocytes

ScopeThe impact of L-ascorbic acid (L-AA) on the chemokinesis (CK) and chemotaxis (CT) of HL-60 cells and polymorphonuclear cells (PMN) was investigated. Methods and resultsHL-60 cells were differentiated with DMSO, retinoic acid (RA), vitamin D, or L-AA. Chemokinesis and chemotaxis of differentiated HL-cells were assayed. Vitamin D3-treated HL-60 cells (dHL-60(vitD3) cells) and RA-treated cells (dHL-60(RA) cells) acquired monocyte/macrophage-like and neutrophil-like phenotypes, respectively. DMSO induced the differentiation of an intermediate phenotype (dHL-60(DMSO) cells), whereas L-AA downregulated neutrophil markers (dHL-60(L-AA) cells). dHL-60(DMSO) cells had increased CK and potent CT in gradients of IL-8 and N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP). dHL-60(RA) cells and dHL-60(L-AA) cells migrated less toward IL-8 and fMLP; dHL-60(vitD3) cells preferably responded to fMLP. L-AA enhanced CK of dHL-60(DMSO) cells and was a weak chemo-attractant. In human leukocytes, IL-8 and fMLP triggered receptor-mediated chemotaxis. CXCR2 and fMLPR were downregulated by IL-8 and fMLP, respectively. L-AA stimulated chemotaxis although significantly less than IL-8 and fMLP. IL-8 targeted chemotaxis was enhanced both in HL-60 cells and leukocytes when cells were incubated with L-AA. ConclusionL-AA modulated chemokinesis and had significant chemo-attractant properties, which were independent on fMLP or IL-8 receptors. The results suggest that L-AA improves leukocyte function in innate immune responses.