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DeBakey Heart Center, Section of Cardiovascular Sciences, Department of Medicine, The Methodist Hospital, Houston, TX 77030; and
Speros P. Martel Laboratory, Section of Leukocyte Biology, Department of Pediatrics, Texas Children’s Hospital, Baylor College of Medicine, Houston, TX 77030
Reperfusion of the ischemic myocardium is associated with a
dramatic inflammatory response leading to TNF-
release, IL-6
induction, and subsequent neutrophil-mediated cytotoxic injury. Because
inflammation is also an important factor in cardiac repair, we
hypothesized the presence of components of the inflammatory reaction
with a possible role in suppressing acute injury. Thus, we investigated
the role of IL-10, an anti-inflammatory cytokine capable of
modulating extracellular matrix biosynthesis, following an experimental
canine myocardial infarction. Using our canine model of myocardial
ischemia and reperfusion, we demonstrated significant up-regulation of
IL-10 mRNA and protein in the ischemic and reperfused myocardium. IL-10
expression was first detected at 5 h and peaked following 96–120
h of reperfusion. In contrast, IL-4 and IL-13, also associated with
suppression of acute inflammation and macrophage deactivation, were not
expressed. In the ischemic canine heart, CD5-positive lymphocytes were
the predominant source of IL-10 in the myocardial infarct. In the
absence of reperfusion, no significant induction of IL-10 mRNA was
noted. In addition, IL-12, a Th1-related cytokine associated with
macrophage activation, was not detected in the ischemic myocardium. In
vitro experiments demonstrated late postischemic cardiac-lymph-induced
tissue inhibitor of metalloproteinases (TIMP)-1 mRNA expression in
isolated canine mononuclear cells. This effect was inhibited when the
incubation contained a neutralizing Ab to IL-10. Our findings suggest
that lymphocytes infiltrating the ischemic and reperfused myocardium
express IL-10 and may have a significant role in healing by modulating
mononuclear cell phenotype and inducing TIMP-1
expression.
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