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Neutrophil-independent mechanisms of caspase-1– and IL-18–mediated ischemic acute tubular necrosis in mice
Open accessAbstract
Having recently described the injurious role of caspase-1-mediated production of the proinflammatory cytokine IL-18 in ischemic acute renal failure (ARF), we report here on the effect of the newly developed caspase inhibitor Quinoline-Val-Asp(Ome)-CH 2 -OPH (OPH-001) on caspase-1, IL-18, neutrophil infiltration, and renal function in ischemic ARF.C57BL/6 mice with ischemic ARF treated with OPH-001 had a marked (100%) reduction in blood urea nitrogen (BUN) and serum creatinine and a highly significant reduction in morphological acute tubular necrosis (ATN) score compared with vehicle-treated mice.OPH-001 significantly reduced the increase in caspase-1 activity and IL-18 and prevented neutrophil infiltration in the kidney during ischemic ARF.To evaluate whether this lack of neutrophil infiltration was contributing to the protection against ischemic ARF, a model of neutrophil depletion was developed.Neutrophil-depleted mice had a small (18%) reduction in serum creatinine during ischemic ARF but no reduction in ATN score despite a lack of neutrophil infiltration in the kidney.Remarkably, caspase-1 activity and IL-18 were significantly increased in the kidney in neutrophil-depleted mice with ARF.In addition, IL-18 antiserum-treated neutrophil-depleted mice with ischemic ARF had a significant (75%) reduction in serum creatinine and a significant reduction in ATN score compared with vehicletreated neutrophil-depleted mice.These results suggest a novel neutrophil-independent mechanism of IL-18-mediated ischemic ARF.
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Cited by
Urinary IL-18 is an early predictive biomarker of acute kidney injury after cardiac surgery
Parikh, C. R., Mishra, J., Thiessen-Philbrook, H., Dursun, B., Ma, Q., Kelly, C., Dent, C., Devarajan, P., & Edelstein, C. L. (2006) · Kidney International · doi:10.1038/sj.ki.5001527 · Cited by 608
Self-citationThe Inflammasomes in Kidney Disease
Anders, H.-J., & Muruve, D. A. (2011) · Journal of the American Society of Nephrology · doi:10.1681/asn.2010080798 · Cited by 351
Cellular and molecular pathways of renal repair after acute kidney injury
Kumar, S. (2018) · Kidney International · doi:10.1016/j.kint.2017.07.030 · Cited by 271
Devarajan, P., Mishra, J., Supavekin, S., Patterson, L. T., & Steven Potter, S. (2003) · Molecular Genetics and Metabolism · doi:10.1016/j.ymgme.2003.09.012 · Cited by 229
Furuichi, K., Gao, J.-L., Horuk, R., Wada, T., Kaneko, S., & Murphy, P. M. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.181.12.8670 · Cited by 100
Metadata
- Authors
- Melnikov, V. Y., Faubel, S., Siegmund, B., Lucia, M. S., Ljubanovic, D., & Edelstein, C. L.
- Venue
- Journal of Clinical Investigation
- Published
- 2002-10-15
- Volume
- 110
- Issue
- 8
- Pages
- 1083-1091
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W4255535345
- Cited by
- 316
- References
- 0
- FWCI
- 6.38
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Melnikov, V. Y., Faubel, S., Siegmund, B., Lucia, M. S., Ljubanovic, D., & Edelstein, C. L. (2002). Neutrophil-independent mechanisms of caspase-1– and IL-18–mediated ischemic acute tubular necrosis in mice. Journal of Clinical Investigation. https://doi.org/10.1172/jci0215623
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