Oxygen and surgical site infection: a study of underlying immunologic mechanisms.
BACKGROUND
Recent clinical trials investigating the role of hyperoxia in decreasing surgical site infection have reported conflicting results. Immunologic mechanisms through which supplemental oxygen could act have not been elucidated fully. The authors sought to investigate the effects of hyperoxia on previously tested and prognostically significant innate immune parameters to uncover the potential effects of hyperoxia at the cellular level.


METHODS
After formal approval and informed consent, venous blood samples were collected from young healthy volunteers. Corresponding samples were incubated at 21 or 80% O2 following a 1 ng/ml lipopolysaccharide challenge and analyzed to determine human leukocyte antigen-DR surface receptor expression, cytokine release, phagocytic capacity, and formation of reactive oxygen species. Data are presented as mean +/- SD.


RESULTS
After the 2 h of incubation at 21% O2 (room air) and in 80% O2 chambers, the change in human leukocyte antigen-DR mean channel fluorescence in lipopolysaccharide-stimulated monocytes was 2,177 +/- 383 and 2,179 +/- 338 (P = 0.96), respectively. Tumor necrosis factor-alpha concentrations were significantly lower for samples incubated at 80% O2 when compared with 21% O2 (P < 0.05). The phagocytic capacity of the innate immune system was not significantly enhanced by supplemental oxygen. However, the formation of reactive oxygen species increased by 87% (P < 0.05).


CONCLUSIONS
Hyperoxia exerts significant effects on multiple cellular and immunologic parameters, providing a potential mechanism for benefits from the use of supplemental oxygen. However, the ability to translate positive basic scientific findings to the operating suite or bedside require the existence of similar innate immune processes in vivo and the efficient transfer of oxygen to the sites where it may be used.
Qadan
Motaz
M
The Price Institute of Surgical Research, University of Louisville School of Medicine, Louisville, Kentucky, USA. mqadan@standford.edu
Battista
Christopher
C
Gardner
Sarah A
SA
Anderson
Gary
G
Akca
Ozan
O
Polk
Hiram C
HC
D000293:Adolescent; D000328:Adult; D017951:Antigen Presentation / Q000187:drug effects / Q000276:immunology; D002634:Chemotaxis, Leukocyte / Q000276:immunology*; D016207:Cytokines / Q000096:biosynthesis / Q000097:blood; D005260:Female; D006684:HLA-DR Antigens / Q000096:biosynthesis / Q000097:blood; D006801:Humans; D018496:Hyperoxia / Q000276:immunology* / Q000517:prevention & control; D007113:Immunity, Innate / Q000187:drug effects; D008297:Male; D009000:Monocytes / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D010100:Oxygen / Q000008:administration & dosage* / Q000097:blood; D010587:Phagocytosis / Q000276:immunology; D011183:Postoperative Complications / Q000097:blood / Q000276:immunology / Q000517:prevention & control; D017382:Reactive Oxygen Species / Q000097:blood / Q000378:metabolism; D015203:Reproducibility of Results; D013530:Surgical Wound Infection / Q000097:blood / Q000276:immunology* / Q000517:prevention & control; D055815:Young Adult
D016207:Cytokines; D006684:HLA-DR Antigens; D017382:Reactive Oxygen Species; D010100:Oxygen