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Hyperbaric oxygen treatment reduces neutrophil‐endothelial adhesion in chronic wound conditions through S ‐nitrosation
Author(s) -
Kendall Alexandra C.,
Whatmore Jacqueline L.,
Winyard Paul G.,
Smerdon Gary R.,
Eggleton Paul
Publication year - 2013
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/wrr.12108
Subject(s) - cell adhesion molecule , umbilical vein , cd18 , cell adhesion , chemistry , wound healing , inflammation , endothelial stem cell , adhesion , tumor necrosis factor alpha , lipopolysaccharide , endothelium , integrin alpha m , nitric oxide , immunology , pharmacology , medicine , biochemistry , cell , in vitro , organic chemistry
Hyperbaric oxygen ( HBO ) therapy is an effective treatment for diabetic chronic wounds. HBO reduces inflammation and accelerates wound healing, by mechanisms that remain unclear. Here we examined a mechanism by which HBO may reduce neutrophil recruitment, through changes in endothelial and neutrophil adhesion molecule expression and function. Human umbilical vein endothelial cells and neutrophils were exposed to selected chronic wound conditions, comprising hypoxia in the presence of lipopolysaccharide and tumor necrosis factor‐alpha, and then treated with HBO . We observed neutrophil adhesion to endothelial cells following treatment with chronic wound conditions, which was reversed by HBO treatment. This was partly explained by reduced expression of endothelial intercellular adhesion molecule‐1 and vascular cell adhesion molecule‐1 by HBO . No changes in neutrophil adhesion molecule expression ( CD18 , CD11b , CD62L , CD31 ) were observed following HBO treatment. However, HBO decreased hydrogen peroxide generation by neutrophils, and induced nitrous oxide–related protein modifications. The transnitrosating agent S ‐nitroso‐ L ‐cysteine ethyl ester (600 μM) also reduced neutrophil adhesion to human umbilical vein endothelial cell monolayers, and the iNOS inhibitor 1400 W (10 μM) and HgCl 2 , which promotes the decomposition of S ‐nitrosothiols (1 mM), reversed the effect of HBO , suggesting that S ‐nitrosation may inhibit neutrophil‐endothelial cell adhesion. This study indicates that HBO could reduce inflammation in wounds through reduced neutrophil recruitment, mediated by S ‐nitrosation.