脂多糖会导致派尔集合淋巴结萎缩，并使共刺激配体CD28和B7的表达增加。

Lipopolysaccharide causes atrophy of Peyer's patches and an increased expression of CD28 and B7 costimulatory ligands.

作者信息

Manhart N, Vierlinger K, Habel O, Bergmeister L H, Götzinger P, Sautner T, Spittler A, Boltz-Nitulescu G, Marian B, Roth E

机构信息

Department of Surgical Research, University of Vienna, Austria.

出版信息

Shock. 2000 Oct;14(4):478-83. doi: 10.1097/00024382-200014040-00010.

DOI:10.1097/00024382-200014040-00010

PMID:11049113

Abstract

Intestinal mucosal dysfunction appears to contribute to infectious complications in critically ill patients. The current study was undertaken to investigate whether endotoxin affects lymphocyte subpopulations and the expression of costimulatory signals in Peyer's patches (PP). Female Balb/c mice were given an intraperitoneal injection of 25 microg LPS and sacrified 24 h or 72 h later to determine total cell yield, lymphocyte subpopulations (B-cells, total T-cells, CD4+- and CD8+-cells), the costimulatory molecules CD28, B7.1 (CD80) and B7.2 (CD86) and the percentage of apoptotic cells in PP and in the spleen as well as small intestinal IgA concentration. Lipopolysaccharide (LPS) challenge caused a significant decrease of total cell yield in PP at both time-points (-50+/-28% and -43+/-25%, respectively; P < 0.001). This decrease was significant for all measured lymphocyte subpopulations. In contrast, total cell yield was increased (P < 0.001) in the spleen 24 h (+52+/-13%) and 72 h (+130+/-22%) after LPS. The decrease of lymphocyte numbers in the PP was accompanied by an increased percentage of lymphocytes expressing costimulatory molecules. In this respect, an increased percentage of CD40+CD80+, CD40+CD86+, and of CD4+CD28+ could be demonstrated after LPS administration. In the spleen, the percentage of CD4+CD28+ was also elevated after LPS bolus, however, the percentage of CD40+CD80+ was reduced, and that of CD40+CD86+ was unaltered. The influence of LPS on apoptosis of lymphocytes was time-dependent. The percentage of apoptotic cells 24 h after LPS was increased in PP (P < 0.01), but was unchanged in the spleen. Seventy-two hours after LPS injection, the percentage of apoptotic cells returned to normal in PP. Luminal IgA levels remained unchanged after LPS challenge. In conclusion, our data show that LPS causes atrophy of PP which seems to be counterregulated by an enhanced expression of costimulatory molecules.

摘要

肠黏膜功能障碍似乎会导致重症患者出现感染性并发症。本研究旨在调查内毒素是否会影响派尔集合淋巴结（PP）中淋巴细胞亚群以及共刺激信号的表达。给雌性Balb/c小鼠腹腔注射25微克脂多糖，24小时或72小时后处死，以测定总细胞产量、淋巴细胞亚群（B细胞、总T细胞、CD4⁺和CD8⁺细胞）、共刺激分子CD28、B7.1（CD80）和B7.2（CD86）以及PP和脾脏中凋亡细胞的百分比，以及小肠中IgA的浓度。脂多糖（LPS）刺激在两个时间点均导致PP中总细胞产量显著下降（分别为-50±28%和-43±25%；P<0.001）。所有测量的淋巴细胞亚群均出现这种下降。相比之下，LPS后24小时（+52±13%）和72小时（+130±22%）脾脏中的总细胞产量增加（P<0.001）。PP中淋巴细胞数量的减少伴随着表达共刺激分子的淋巴细胞百分比增加。在这方面，LPS给药后可证明CD40⁺CD80⁺、CD40⁺CD86⁺以及CD4⁺CD28⁺的百分比增加。在脾脏中，LPS推注后CD4⁺CD28⁺的百分比也升高，但CD40⁺CD80⁺的百分比降低，而CD40⁺CD86⁺的百分比未改变。LPS对淋巴细胞凋亡的影响具有时间依赖性。LPS后24小时PP中凋亡细胞的百分比增加（P<0.01），但脾脏中未改变。LPS注射72小时后，PP中凋亡细胞的百分比恢复正常。LPS刺激后管腔内IgA水平保持不变。总之，我们的数据表明，LPS导致PP萎缩，这似乎通过共刺激分子表达的增强而得到反向调节。