Hyperbaric oxygen exposure temporarily reduces Mac-1 mediated functions of human neutrophils.
Highly elevated partial pressures of oxygen achievable during hyperbaric oxygenation (HBO) have been shown to reduce leukocyte sequestration following ischemia/reperfusion injury suggesting a clinical role for HBO in treatment of various disease states characterized by transient ischemia. Previous studies have suggested that this effect may be due to inhibition of beta2-integrin function. In this study the effect of HBO on various CD11b/CD18 (Mac-1) mediated neutrophil functions was investigated in healthy human subjects. HBO 3.0 ATA, 23 m reduced adhesion 50% at 2 h with return to pre-HBO levels by 6 h. Homotypic aggregation, a Mac-1 dependent function, under fluid shear following stimulation with f-MLP was reduced from 20+/-2.6 to 3.4+/-1.0% 2 h after HBO. However, HBO did not inhibit adhesion to IL-1beta stimulated HUVEC. Mac-1 mediated oxidative burst induced by opsonized zymosan was reduced 38.2+/-10.6% (P<0.05) by HBO. However, oxidative burst induced by PMA or f-MLP was not affected. HBO did not alter the distribution of neutrophils displaying morphologies associated with stimulation (ruffled, bipolar, uropod) over a 24 h period after HBO nor did HBO change the percentages of mature versus immature cells. Taken together these findings demonstrate that HBO specifically inhibits Mac-1 mediated functions.
Kalns
John
J
Davis Hyperbaric Laboratory, Brooks AFB, TX 78235, USA. john.kalns@brooks.af.mil
Lane
Janae
J
Delgado
Angel
A
Scruggs
Julie
J
Ayala
Eleanor
E
Gutierrez
Elizabeth
E
Warren
Doug
D
Niemeyer
Debra
D
George Wolf
E
E
Bowden
Robert A
RA
D006801:Humans; D006931:Hyperbaric Oxygenation; D066298:In Vitro Techniques; D016177:Macrophage-1 Antigen / Q000378:metabolism*; D009504:Neutrophils / Q000378:metabolism* / Q000473:pathology; D016897:Respiratory Burst
D016177:Macrophage-1 Antigen