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Published ahead of print on February 2, 2005
J Am Soc Nephrol 16: 720-728, 2005
© 2005 American Society of Nephrology
doi: 10.1681/ASN.2004050381
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Pathophysiology of Renal Disease and Progression

T Cells Modulate Neutrophil-Dependent Acute Renal Failure during Endotoxemia: Critical Role for CD28

Kai Singbartl, Susanne Große Bockhorn, Alexander Zarbock, Mirco Schmolke and Hugo Van Aken

Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Universitätsklinikum, Münster, Germany

Address correspondence to: Dr. Kai Singbartl, Klinik und Poliklinik für Anästhesiologie und operative Intensivmedizin, Universitätsklinikum Münster, Albert Schweitzer Strasse 33, 48129 Münster, Germany. Phone: +49-251-980-2472; Fax: +49-251-980-2473; E-mail: singbartl{at}uni-muenster.de

Sepsis still represents a leading cause of acute renal failure (ARF). Both lymphocytes and neutrophils (PMN) have been proposed as crucial mediators during sepsis. For further elucidation of the mechanisms of interactions between them, a murine model of LPS-induced ARF was used. In wild-type mice (WT), LPS administration led to a strong influx of PMN into the kidney (2.8-fold greater renal myeloperoxidase activity after 24 h) and to severe ARF (3.3-fold higher plasma creatinine concentrations after 24 h). By contrast, mice that were gene deficient for CD28 (CD28–/–), a co-stimulatory molecule for T cell activation, exhibited only minor renal dysfunction (50% protection compared with WT) and almost no PMN recruitment. When PMN– depleted, both WT and CD28–/– developed only mild ARF, similar to untreated CD28–/–. Flow cytometry demonstrated that CD28 was vastly expressed on CD3+ cells but not on PMN. Injecting wild-type CD3+ cells into CD28–/– before LPS injection abolished the protection seen before. At baseline, both WT and CD28–/– displayed similar plasma concentrations of keratinocyte-derived chemokine (KC), a growth-related oncogene 1 gene product and PMN-specific chemokine. As opposed to WT, CD28–/– showed a greatly attenuated increase in plasma KC 4 h after LPS (2.5- versus 138.5-fold over controls, respectively). Moreover, CD28–/– showed less intense upregulation of renal growth-related oncogene 1 mRNA expression. Immunohistochemistry revealed considerable PMN but no T cell infiltrates in the kidney after LPS injection. In a PMN-dependent model of endotoxemic ARF, T cells, via the CD28 pathway, modulate kidney function and renal PMN recruitment. The effect on PMN is a remote one and presumably due to altered expression of PMN-specific chemokines.


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