Pattern recognition receptors (PRRs) are potent triggers of tissue injury following renal ischemia/reperfusion injury (IRI). Specific PRRs, such as the toll-like receptor 2 (TLR2) and the nucleotide-binding oligomerization domain-like receptors (NLRs) NOD1 and NOD2 are promising targets to abrogate inflammatory injury associated with renal IRI. Several recent reports have shown there is crosstalk between TLRs and NODs, which might boost inflammatory responses to tissue injury. This study examined the relative roles of TLR2 and NODs 1 and 2 in activation of myeloid cells that contribute to inflammation after renal IRI. We found that TLR2 and NOD1 and 2 signaling induces neutrophil, macrophage and dendritic cell migration in vitro, however their blockade only decreases neutrophil infiltration into ischemic kidneys. The results of this study suggest that future therapies targeted to innate immune blockade should consider that either TLR2 or NOD1/2 blockade could decrease neutrophil inflammation following an ischemic insult to the kidney, however blockade of these PRRs would not likely impact infiltration of dendritic cells or macrophages. Developing rational approaches that target innate immunity in IRI-induced acute kidney injury requires an understanding of the relative role of PRRs in directing inflammation in the kidney.

模式识别受体（PRR）是肾缺血/再灌注损伤（IRI）后组织损伤的有效触发因素。特定的 PRR，例如 Toll 样受体 2 (TLR2) 和核苷酸结合寡聚化结构域样受体 (NLR) NOD1 和 NOD2，是消除与肾 IRI 相关的炎症损伤的有希望的靶标。最近的几份报告表明，TLR 和 NOD 之间存在串扰，这可能会增强对组织损伤的炎症反应。本研究探讨了 TLR2 以及 NOD 1 和 2 在导致肾 IRI 后炎症的骨髓细胞激活中的相对作用。我们发现 TLR2 和 NOD1 和 2 信号传导在体外诱导中性粒细胞、巨噬细胞和树突状细胞迁移，但它们的阻断仅减少中性粒细胞浸润到缺血肾脏。这项研究的结果表明，未来针对先天免疫阻断的治疗应考虑 TLR2 或 NOD1/2 阻断可以减少肾脏缺血性损伤后的中性粒细胞炎症，但阻断这些 PRR 不太可能影响树突状细胞或树突状细胞的浸润。巨噬细胞。开发针对 IRI 诱导的急性肾损伤先天免疫的合理方法需要了解 PRR 在引导肾脏炎症中的相对作用。