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Nephrol Dial Transplant (2000) 15: 1556-1561
© 2000 European Renal Association-European Dialysis and Transplant Association

Antibody-induced modulation of the leukocyte CD11b integrin prevents mild but not major renal ischaemic injury

Luis C. F. Tajra1,2, Xavier Martin2, Jacqueline Margonari1, Nelly Blanc-Brunat3, Michio Ishibashi1, Geneviève Vivier3, Jean P. Steghens5, Hiroto Kawashima6, Masayuki Miyasaka6, Jean-M. Dubernard2 and Jean-P. Revillard4,

1 INSERM, Unité 281, Laboratoire de Recherche Chirurgicale, 2 Service d'Urologie et Chirurgie de la Transplantation, 3 INSERM, Laboratoire d'Immunopathologie, 4 INSERM, Unité 503, Immuno-Biologie Fondamentale et Clinique, 5 Laboratoire de Biochimie, Hôpital Edouard Herriot, Lyon, France, and 6 Department of Bioregulation, Biomedical Research Center, Osaka University Medical School, Suita, Japan

Background. CD11/CD18 ß2 integrins are involved in leukocyte adhesion to the activated endothelium, and therefore represent a possible therapeutic target in the prevention of ischaemic acute renal failure (ARF).

Methods. To assess the effect of an anti-CD11b monoclonal antibody (mAb) in ischaemic ARF, uninephrectomized Fischer rats were subjected to 45 or 60 min of warm renal ischaemia, then received 1 mg of anti-CD11b mAb 5 min before reperfusion.

Results. After 45 min of ischaemia, renal function tests at 24 and 48 h were less altered in mAb-treated than in control rats, but after 60 min of ischaemia the same level of renal insufficiency was observed in the two groups. In parallel, milder tubular necrosis and less leukocyte infiltration were observed in the treated group after 45 min of ischaemia, but no difference was seen after 60 min compared to the control group. The mAb was detected on blood neutrophils up to 48 h after infusion and a marked down-regulation of CD11b expression on neutrophil surfaces was documented by flow cytometry.

Conclusion. These results indicate that anti-CD11b mAb administered prior to reperfusion decreases moderate ischaemic ARF but fails to prevent renal injury secondary to prolonged ischaemia in this model.

Keywords: adhesion molecules; integrins; Mac-1; monoclonal antibody; rat; renal ischaemic injury

Correspondence and offprint requests to: Professor J. P. Revillard, INSERM, Unite 503, Immuno-Biologie Fondamentale et Clinique Hôpital Edouard Herriot, Place d'Arsonval, F-69437 Lyon Cedex 3, France.


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