Konttinen Y T, Hukkanen M, Segerberg M, Rees R, Kemppinen P, Sorsa T, Saari H, Polak J M, Santavirta S
Institute of Molecular Immunology, NYU Medical Center, New York.
Scand J Rheumatol. 1992;21(2):55-9. doi: 10.3109/03009749209095068.
The purpose of this study was to assess the relationship of neuropeptide nerves and inflammatory leukocytes in PVG rats with adjuvant-induced arthritis. Substance P- and calcitonin gene-related peptide (CGRP)-immunoreactive nerves and inflammatory leukocytes were studied, using peroxidase (ABC) and/or alkaline phosphatase (APAAP) staining. Inflamed synovial tissue proper was infiltrated with neutrophils, ED1 macrophages and focal accumulations of CD2 T lymphocytes. In such tissue, the relationship between peptide-immunoreactive nerves and inflammatory cells was such that substance P and CGRP nerves were absent in heavily infiltrated villous synovial tissue, whereas healthy synovial tissue and non-inflammatory areas in adjuvant arthritic rats were innervated by substance P and CGRP nerves close to normal synovial tissue resident cells. In order to elucidate an eventual mechanism for lost immunoreactivity, healthy synovial tissue was exposed to chymotrypsin or oxygen derived free radicals (ODFR) in vitro. The former treatment caused total loss of immunoreactivity. These findings suggest that neuropeptides and neuropeptide containing nerves may be destroyed by locally produced proteolytic enzymes and various reactive oxygen species in the vicinity of inflammatory cells.
本研究的目的是评估佐剂诱导性关节炎PVG大鼠中神经肽神经与炎性白细胞之间的关系。采用过氧化物酶（ABC）和/或碱性磷酸酶（APAAP）染色法，对P物质和降钙素基因相关肽（CGRP）免疫反应性神经以及炎性白细胞进行了研究。炎症性滑膜组织固有层有中性粒细胞、ED1巨噬细胞浸润以及CD2 T淋巴细胞的局灶性聚集。在这样的组织中，肽免疫反应性神经与炎性细胞之间的关系是，在重度浸润的绒毛状滑膜组织中不存在P物质和CGRP神经，而佐剂性关节炎大鼠的健康滑膜组织和非炎症区域由靠近正常滑膜组织驻留细胞的P物质和CGRP神经支配。为了阐明免疫反应性丧失的潜在机制，将健康滑膜组织在体外暴露于胰凝乳蛋白酶或氧衍生自由基（ODFR）。前一种处理导致免疫反应性完全丧失。这些发现表明，神经肽和含神经肽的神经可能被炎性细胞附近局部产生的蛋白水解酶和各种活性氧所破坏。
