来自感染猴免疫缺陷病毒（SIV）的猴子的外周血单核细胞/巨噬细胞中喹啉酸免疫反应性增加。

Increased quinolinate immunoreactivity in the peripheral blood monocytes/macrophages from SIV-infected monkeys.

作者信息

Namboodiri A M, Venkateshan C N, Narayanan R, Blinder K, Moffett J R, Gajdusek D C, Gravell M, Gibbs C J

机构信息

Department of Biology, Georgetown University, Washington DC 20057, USA.

出版信息

J Neurovirol. 1996 Dec;2(6):433-8. doi: 10.3109/13550289609146910.

DOI:10.3109/13550289609146910

PMID:8972426

Abstract

Quinolinate (QUIN), a metabolite in the kynurenine pathway of tryptophan degradation and a neurotoxin that is thought to act through the NMDA receptor system, was localized in cultured peripheral blood monocytes/macrophages from SIV-infected monkeys using a recently developed immunohistochemical method. Significant increases in QUIN immunoreactive (IR) cells were detected in all five SIV-infected monkeys examined. Multinucleated giant cells, a hallmark of lentiviral infection, were visible in selected samples. Treatment with the QUIN precursors, tryptophan and kynurenine, increased the number of QUIN-IR cells in both the control and SIV-infected preparations, perhaps by a mass action mechanism. We hypothesize that in SIV-infected monkeys, infiltrating monocytes/macrophages contribute to the high level of brain QUIN and associated neuropathology.

摘要

喹啉酸（QUIN）是色氨酸降解犬尿氨酸途径中的一种代谢产物，是一种被认为通过N-甲基-D-天冬氨酸（NMDA）受体系统发挥作用的神经毒素。利用最近开发的免疫组织化学方法，在感染猴免疫缺陷病毒（SIV）的猴子的培养外周血单核细胞/巨噬细胞中对其进行了定位。在所检查的所有五只感染SIV的猴子中，均检测到喹啉酸免疫反应性（IR）细胞显著增加。在选定的样本中可见多核巨细胞，这是慢病毒感染的一个标志。用喹啉酸前体色氨酸和犬尿氨酸进行处理，增加了对照和感染SIV制剂中喹啉酸免疫反应细胞的数量，这可能是通过质量作用机制实现的。我们推测，在感染SIV的猴子中，浸润的单核细胞/巨噬细胞导致了大脑中高水平的喹啉酸及相关神经病理学变化。