Quantification and localization of M2 macrophages in human kidneys with acute tubular injury.
Quantification and localization of M2 macrophages in human kidneys with acute tubular injury.
复制标题
急性管状损伤的人肾中M2巨噬细胞的定量和定位。
DOI：
10.2147/ijnrd.s66936
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发表时间：
2014
影响因子：
2
通讯作者：
Moeckel GW
中科院分区：
文献类型：
--
作者：
Palmer MB;Vichot AA;Cantley LG;Moeckel GW
这项研究首次提出在急性肾小管损伤(ATI)患者的肾脏切片中是否存在显著的巨噬细胞群的问题。因此，我们检查了经活检证实为ATI、微小病变病(MCD)和MCD伴ATI的人肾组织中的间质巨噬细胞群。用CD68(一般巨噬细胞标志物)、CD163(M2标志物)和HLA-DR(M1标志物)抗体对上述诊断的患者的肾活检组织进行染色，并对其相应的电子显微镜标本进行间质巨噬细胞的检测。我们的研究表明，与单纯MCD患者相比，ATI患者间质CD68+巨噬细胞数量显著增加，其中HLA-DR+M1巨噬细胞和CD163+M2巨噬细胞均增加。大约75%的巨噬细胞是M2(CD163+)，而只有25%的巨噬细胞是M1(HLA-DR+)。M2巨噬细胞被认为是伤口愈合的关键，它位于受损近端小管细胞的肾小管基底膜附近。超微结构检查显示巨噬细胞与损伤的肾小管上皮细胞基底膜紧密粘连。我们得出结论，在ATI后，巨噬细胞聚集在受损的小管周围，并主要表现为M2表型。我们进一步推测，巨噬细胞介导的修复可能涉及M2巨噬细胞与受损的肾小管上皮细胞之间的物理接触。
This study addresses for the first time the question whether there is significant macrophage population in human kidney sections from patients with acute tubular injury (ATI). We examined therefore the interstitial macrophage population in human kidney tissue with biopsy-proven diagnosis of ATI, minimal change disease (MCD), and MCD with ATI. Kidney biopsies from patients with the above diagnoses were stained with antibodies directed against CD68 (general macrophage marker), CD163 (M2 marker), and HLA-DR (M1 marker) and their respective electron microscopy samples were evaluated for the presence of interstitial macrophages. Our study shows that patients with ATI have significantly increased numbers of interstitial CD68+ macrophages, with an increase in both HLA-DR+ M1 macrophages and CD163+ M2 macrophages as compared to patients with MCD alone. Approximately 75% of macrophages were M2 (CD163+) whereas only 25% were M1 (HLA-DR+). M2 macrophages, which are believed to be critical for wound healing, were found to localize close to the tubular basement membrane of injured proximal tubule cells. Ultra structural examination showed close adherence of macrophages to the basement membrane of injured tubular epithelial cells. We conclude that macrophages accumulate around injured tubules following ATI and exhibit predominantly an M2 phenotype. We further speculate that macrophage-mediated repair may involve physical contact between the M2 macrophage and the injured tubular epithelial cell.