From the Department of Otolaryngology, Nippon Medical School, Sendagi, Bunkyo-ku, Tokyo, Japan.
World Allergy Organ J. 2009 Oct;2(10):218-23. doi: 10.1097/WOX.0b013e3181bdd219.
: Accumulation of T cells and immature dendritic cells (DCs) is one of the characteristic features of nasal polyps. However, the question remains why these cells accumulate in nasal polyp tissue. Macrophage inflammatory protein-3α; (MIP-3α;/CCL20) is a chemokine involved in the migration of T cells and immature DCs into inflammatory tissue sites. Fibroblasts are a rich source of cytokines and chemokines. The objective of this study was to demonstrate the expression of MIP-3α;/CCL20 in nasal polyp fibroblasts after stimulation with proinflammatory cytokines such as interleukin-17 (IL-17) and tumor necrosis factor-α; (TNF-α;).
: Fibroblast lines were established from nasal polyps. MIP-3α;/CCL20 mRNA expression was evaluated by real-time reverse transcription-polymerase chain reaction (real-time RT-PCR). The amount of MIP-3α;/CCL20 in the supernatants was measured by enzyme-linked immunosorbent assay (ELISA).
: IL-17A and TNF-α; synergistically induced MIP-3α;/CCL20 production by nasal polyp fibroblasts in a dose- and time-dependent manner. This synergy was observed by stimulation with TNF-α; plus IL-17A or IL-17F, but not IL-17E.
: Nasal polyp fibroblasts, by producing MIP-3α;/CCL20, may play an important role in the recruitment of T cells and DCs in upper airway inflammatory lesions such as nasal polyps.
T 细胞和未成熟树突状细胞（DC）的积累是鼻息肉的特征之一。然而，这些细胞为什么会在鼻息肉组织中积累仍然是一个问题。巨噬细胞炎症蛋白-3α（MIP-3α；/CCL20）是一种趋化因子，参与 T 细胞和未成熟 DC 向炎症组织部位的迁移。成纤维细胞是细胞因子和趋化因子的丰富来源。本研究旨在证明在促炎细胞因子（如白细胞介素 17（IL-17）和肿瘤坏死因子-α；（TNF-α；）刺激后，鼻息肉成纤维细胞中 MIP-3α；/CCL20 的表达。
从鼻息肉中建立成纤维细胞系。通过实时逆转录聚合酶链反应（real-time RT-PCR）评估 MIP-3α；/CCL20 mRNA 表达。通过酶联免疫吸附试验（ELISA）测量上清液中 MIP-3α；/CCL20 的量。
IL-17A 和 TNF-α；以剂量和时间依赖的方式协同诱导鼻息肉成纤维细胞产生 MIP-3α；/CCL20。通过刺激 TNF-α；加 IL-17A 或 IL-17F 观察到这种协同作用，但不是通过刺激 IL-17E。
鼻息肉成纤维细胞通过产生 MIP-3α；/CCL20，可能在上呼吸道炎症病变（如鼻息肉）中在招募 T 细胞和 DC 方面发挥重要作用。
