The macrophage system in the intestinal muscularis externa during inflammation: an immunohistochemical and quantitative study of osteopetrotic mice
The macrophage system in the intestinal muscularis externa during inflammation: an immunohistochemical and quantitative study of osteopetrotic mice
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DOI：
10.1007/s00418-008-0423-x
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发表时间：
2008-08-01
影响因子：
2.3
通讯作者：
Hadberg, H.
中科院分区：
文献类型：
--
作者：
Mikkelsen, H. B.;Larsen, J. O.;Hadberg, H.
肠道炎症会导致人类和动物模型的肠道蠕动紊乱。平滑肌细胞和/或肠神经系统的这种功能改变可能是由于外肌层巨噬细胞的活化以及细胞因子和趋化因子的释放引起的，导致单核细胞和中性粒细胞的流入。我们对缺乏某些巨噬细胞亚型的骨石症（op/op）小鼠进行了实验，例如巨噬细胞亚型。外肌层和+/+小鼠的巨噬细胞接触LPS以诱导炎症细胞流入。使用体视取样对 F4/80(+)、MHCII+ 和髓过氧化物酶 (+) 细胞的密度进行定量。在+/+小鼠中，我们发现MHCII+细胞的数量多于F4/80(+)细胞，并且LPS注射暂时增加了MHCII+细胞的密度，但没有增加F4/80(+)细胞的密度。这表明 MHCII 抗原发生上调，并且存在两种或更多种具有相似形态的巨噬细胞亚型。骨质疏松小鼠在任一治疗后均缺乏MHCII+、CD169(+)和F4/80(+)细胞，这表明这些细胞是CSF-1依赖性的。在 +/+ 和 op/op 小鼠中，LPS 诱导血管的 VCAM-1 激活、粒细胞的适度流入以及不同于巨噬细胞的细胞类型的 iNOS 激活。
Intestinal inflammation results in disturbed intestinal motility in humans as well as in animal models. This altered function of smooth muscle cells and/or the enteric nervous system may be caused by activation of macrophages in muscularis externa and a thereby following release of cytokines and chemokines that causes influx of mononuclear cells and neutrophilic granulocytes. We subjected osteopetrotic (op/op) mice that lack certain macrophage subtypes, e.g. macrophages in the muscularis externa and +/+ mice to LPS to induce inflammatory cell influx. The densities of F4/80(+), MHCII+, and myeloperoxidase(+) cells were quantified using stereological sampling. In +/+ mice we found that MHCII+ cells outnumber F4/80(+) cells and that LPS injection increased the density of MHCII+ cells temporarily but not that of F4/80(+) cells. This indicates that an upregulation of MHCII antigen takes place and that two or more macrophage subtypes with comparable morphologies exist. Osteopetrotic mice lacked MHCII+, CD169(+), and F4/80(+) cells after either treatment, which indicate that these cells are CSF-1-dependent. LPS induced VCAM-1 activation of the vessels, modest influx of granulocytes, as well as an iNOS-activation in a cell type different from macrophages in both +/+ and op/op mice.