| First Author | Marques VP | Year | 2006 |
| Journal | Nephron Exp Nephrol | Volume | 104 |
| Issue | 1 | Pages | e48-56 |
| PubMed ID | 16741373 | Mgi Jnum | J:127477 |
| Mgi Id | MGI:3763800 | Doi | 10.1159/000093676 |
| Citation | Marques VP, et al. (2006) Influence of TH1/TH2 switched immune response on renal ischemia-reperfusion injury. Nephron Exp Nephrol 104(1):e48-56 |
| abstractText | BACKGROUND/AIMS: Recent evidence shows a critical role of the CD4+ T cell with the Th1/Th2 paradigm as a possible effector mechanism in ischemia and reperfusion injury. We hypothesize that a polarized Th1 activation response may negatively influence the renal IRI through its relationship with chemokine production (MCP-1) and with a protective tissue response (HO-1). METHODS: We subjected mice to renal ischemia for 45 min using IL-4 and IL-12 knockout C57BL/6. We then measured serum urea levels, performed histomorphometric analysis for tubular necrosis and regeneration, and evaluated the mRNA expression of HO-1, t-bet, Gata-3 and MCP-1 by real-time PCR at 24, 48 and 120 h after surgery. RESULTS/CONCLUSIONS: The IL-4 knockout mice had a statistically significant rise in serum urea levels post IRI compared with control animals. The IL-12-deficient mice were not affected. The IL-4-deficient mice had a statistically significant increase in tubular injury and impairment in cell regeneration. The IRI in IL-4-deficient mice was accompanied by higher levels of HO-1, t-bet and later up-regulation of MCP-1. These findings suggest that the deleterious effects of the Th1 cell involve increased production of chemokines such as MCP-1. |
