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Leukocytes, cell adhesion molecules and ischemic acute renal failure
H Rabb1, Y M O'Meara, P Maderna
1Division of Nephrology and Hypertension, University of South Florida, USA.
Abstract:
Ischemic acute renal failure (ARF) is a common clinical syndrome, associated with high morbidity and mortality, for which there is no specific therapy. Polymorphonuclear neutrophils (PMN) recruited during reperfusion have been implicated as mediators of renal parenchymal injury in ischemic ARF. Leukocyte adhesion molecules appear to facilitate PMN recruitment in this setting. Complementary studies using monoclonal antibodies, antisense oligonucleotides and gene "knock-out" indicate that blockade of CD11/CD18 integrins and intercellular adhesion molecule-1 (ICAM-1) attenuates ARF in some experimental models of renal ischemia. These exciting observations may herald the development of novel anti-adhesion strategies for use in human disease.
Insights
Ischemic acute renal failure (ARF) lacks specific therapies. Blocking leukocyte adhesion molecules like CD11/CD18 and ICAM-1 shows promise in reducing kidney injury in experimental models, potentially leading to new treatments.
Area of Science:
- Nephrology
- Immunology
- Pathophysiology
Background:
- Ischemic acute renal failure (ARF) is a significant clinical syndrome with high morbidity and mortality.
- Polymorphonuclear neutrophils (PMN) are implicated in mediating renal parenchymal injury during ischemic ARF.
- Leukocyte adhesion molecules are crucial for PMN recruitment in this context.
Purpose of the Study:
- To investigate the role of leukocyte adhesion molecules in mediating renal injury during ischemic ARF.
- To evaluate the therapeutic potential of blocking specific adhesion molecules in experimental models of renal ischemia.
Main Methods:
- Utilized experimental models of renal ischemia.
- Employed strategies including monoclonal antibodies, antisense oligonucleotides, and gene "knock-out" to block CD11/CD18 integrins and intercellular adhesion molecule-1 (ICAM-1).
Main Results:
- Blockade of CD11/CD18 integrins and ICAM-1 attenuated renal injury in experimental models of ischemic ARF.
- These findings support the involvement of PMN recruitment via adhesion molecules in ischemic kidney damage.
Conclusions:
- Targeting leukocyte adhesion molecules represents a potential therapeutic strategy for ischemic ARF.
- Further development of anti-adhesion therapies may offer novel treatment options for human ARF.