Lipopolysaccharide activates the muscularis macrophage network and suppresses circular smooth muscle activity
Lipopolysaccharide activates the muscularis macrophage network and suppresses circular smooth muscle activity
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DOI：
10.1152/ajpgi.1997.273.3.g727
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发表时间：
1997-09-01
影响因子：
4.5
通讯作者：
Bauer, AJ
中科院分区：
文献类型：
--
作者：
Eskandari, MK;Kalff, JC;Bauer, AJ
细菌脂多糖(LPS)是脓毒症所致肠梗阻的病原体。虽然已知内毒素激活巨噬细胞并引发炎症，但内毒素对巨噬细胞网络和肠道肌层内潜在的炎症反应的影响尚未被研究。本研究旨在探讨腹膜腔内毒素对大鼠肠肌层细胞和功能的影响。用组织化学和免疫组织化学方法检测白细胞表型。用脏器浴法测定功能改变。与对照组相比，注射内毒素后1h，ED2(+)巨噬细胞网络中淋巴细胞活化标记-1(LFA-1)的染色增加了21倍。随后，中性粒细胞、肥大细胞和单核细胞大量渗入肌层。注射后12小时，脂多糖还使自发性环行肌活动减少62%，对儿茶酚刺激的收缩抑制91%。这些结果表明，内毒素血症1)剧烈激活肌层巨噬细胞网络，2)导致白细胞外溢，3)导致环状肌肉损伤。
Bacterial lipopolysaccharide (LPS) is a causative agent of sepsis-induced ileus. Although it is known that LPS activates macrophages and initiates inflammation, the consequences of LPS on the macrophage network and a potential inflammatory response within the intestinal muscularis have not been investigated. This study was designed to identify cellular and functional changes in rat intestinal muscularis after intraperitoneal LPS. Histo- and immunohistochemistry were used to phenotype leukocytes. Functional alterations were determined using an organ bath. Compared with controls, LPS caused a 21-fold increase in staining for the lymphocyte activation marker-1 (LFA-1) localized to the ED2(+) macrophage network 1 h after injection. This was followed by a significant infiltration of neutrophils, mast cells, and monocytes into the muscularis. LPS also caused a 62% reduction in spontaneous circular muscle activity and a 91% suppression of bethanechol-stimulated contractions 12 h after injection. These results demonstrate that endotoxemia 1) acutely activates the muscularis macrophage network, 2) causes the extravasation of leukocytes, and 3) results in circular muscle impairment.