Levels of macrophage migration inhibitory factor and glucocorticoids in chronic wound patients and their potential interactions with impaired wound endothelial progenitor cell migration.
Macrophage migration inhibitory factor (MIF), a structurally and functionally unique pleiotropic mediator in inflammation and immune processes, was identified decades ago. There is now strong evidence that MIF promotes revascularization and is involved in wound healing processes. However, its exact role in wound healing is still a matter of debate. A cohort of 33 patients was recruited, including 14 patients with acute and 19 patients with chronic wounds. Both serum and wound fluid samples were collected from each patient, and MIF and cortisol concentrations were determined. To functionally underscore MIF's potential role in wound revascularization, a chemotaxis assay was adapted to test whether and to what extent serum samples and wound fluids of each group promote the chemotactic migration of endothelial progenitor cells (EPCs). MIF serum levels were significantly higher in chronic wound patients than in acute wound patients. Wound exudates of chronic wounds, however, contained a significantly lower concentration of MIF. In chronic wound patients, EPC migration might be delayed, as suggested by in vitro chemotaxis experiments. Despite the overall descriptive nature of this study, we conclude that MIF is correlated with occurrence of chronic wound. The increased MIF levels in the serum of chronic wound patients might be due to MIF's systemic effect of its proinflammatory activities, while its locally decreased levels in chronic wound exudates might be responsible for impaired recruitment of EPCs. Additional prospective data and detailed in vivo models are needed for a more comprehensive understanding of the role of MIF in chronic wound healing.
Department of Plastic Surgery and Hand Surgery, Burn Center, Medical Faculty, RWTH Aachen University, Aachen, Germany. gerritgrieb@gmx.de
Gerrit
G
Grieb
David
D
Simons
Lena
L
Eckert
Melanie
M
Hemmrich
Guy
G
Steffens
Jürgen
J
Bernhagen
Norbert
N
Pallua
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002465:Cell Movement; D002478:Cells, Cultured; D054377:Chemokine CXCL12 / Q000187:drug effects / Q000276:immunology*; D002633:Chemotaxis / Q000187:drug effects / Q000276:immunology*; D002908:Chronic Disease; D015331:Cohort Studies; D042783:Endothelial Cells / Q000187:drug effects / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D007249:Inflammation; D008263:Macrophage Migration-Inhibitory Factors / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D018919:Neovascularization, Physiologic / Q000187:drug effects / Q000276:immunology; D013234:Stem Cells / Q000187:drug effects / Q000276:immunology*; D014945:Wound Healing / Q000187:drug effects / Q000276:immunology*; D055815:Young Adult
C515255:CXCL12 protein, human; D054377:Chemokine CXCL12; D005938:Glucocorticoids; D008263:Macrophage Migration-Inhibitory Factors