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Department of Internal Medicine and Department of Pharmacology, Cardiovascular Center, University of Iowa College of Medicine, Iowa City, Iowa 52242-1081
Little is known about the role of
interleukin-10 (IL-10), an anti-inflammatory cytokine, in blood
vessels. We used IL-10-deficient mice (IL-10 
/) to examine the
hypothesis that IL-10 protects endothelial function after
lipopolysaccharide (LPS) treatment. The responses of carotid
arteries were studied in vitro 6 h after injection of a relatively
low dose of LPS (10 µg ip). In IL-10 / mice, the maximum
relaxation to ACh (3 µM) was 56 ± 6% (means ± SE) after
LPS injection and 84 ± 4% after vehicle injection (P < 0.05). Thus endothelium-dependent relaxation was
impaired in carotid arteries from IL-10 / mice after LPS injection.
In contrast, this dose of LPS did not alter relaxation to ACh in vessels from wild-type (IL-10 +/+) mice. Relaxation to nitroprusside and papaverine was similar in arteries from both IL-10 / and IL-10
+/+ mice after vehicle or LPS injection. Because inflammation is
associated with increased levels of reactive oxygen species, we also
tested the hypothesis that superoxide contributes to the impairment of
endothelial function by LPS in the absence of IL-10. Results using
confocal microscopy and hydroethidine indicated that levels of
superoxide are elevated in carotid arteries from IL-10 / mice
compared with IL-10 +/+ mice after LPS injection. The impaired
relaxation of arteries from IL-10 / mice after LPS injection was
restored to normal by polyethylene glycol-suspended superoxide
dismutase (50 U/ml) or allopurinol (1 mM), an inhibitor of xanthine
oxidase. These data provide direct evidence that IL-10 protects
endothelial function after an acute inflammatory stimulus by limiting
local increases in superoxide. The source of superoxide in this model
may be xanthine oxidase.
nitric oxide; reactive oxygen species; gene-targeted mice; endothelium-dependent relaxation; interleukin-10
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