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Regular Article |
and Macrophage Inflammatory Protein-2 Attenuates Renal Ischemia/Reperfusion Injury
From the Urological Institute*
and the Department
of Immunology,
Cleveland Clinic Foundation,
Cleveland, Ohio; the Department of Pathology,
Case Western Reserve University School of Medicine, Cleveland, Ohio;
and the Department of Pathology,
University of
Michigan Medical School, Ann Arbor, Michigan
Previous studies have provided strong evidence for a role for
neutrophils in mediating pathology during reperfusion of ischemic
tissues. CXC chemokines including interleukin-8,
KC/Gro
, and macrophage inflammatory protein
(MIP)-2, direct neutrophils to tissue sites of inflammation. In
the current study we tested the efficacy of antibodies to KC/Gro and
MIP-2 in inhibiting neutrophil infiltration into kidneys during
reperfusion after 1 hour of warm ischemia using a mouse model. KC mRNA
and protein were produced within 3 hours after reperfusion of the
ischemic kidneys. MIP-2 mRNA and protein were twofold to fourfold lower
than KC and were at low levels until 9 hours after reperfusion. Only
60% of mice subjected to ischemia/reperfusion injury survived to day 3
after reperfusion. Treatment with rabbit neutralizing antibodies to
both KC and MIP-2 inhibited neutrophil infiltration into ischemic
kidneys during reperfusion, restored renal function as assessed
by decreased serum creatinine and urea nitrogen levels to near normal
levels, and resulted in complete survival of treated animals.
Finally, treatment with both antibodies significantly reduced
histologically graded pathology of kidneys subjected to
ischemia/reperfusion injury. Collectively, the results indicate
the efficacy of neutralizing the chemokines directing neutrophils into
ischemic kidneys during reperfusion to inhibit this infiltration and
attenuate the resulting pathology.
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