Schaefer D, Meyer J E, Pods R, Pethe W, Hedderich J, Schmidt C, Maune S
Department of Allergology Medical Clinic III, Friedrich Alexander University of Erlangen-Nuremberg, Erlangen-Nuremberg, Germany.
Int Arch Allergy Immunol. 2006;140(3):205-14. doi: 10.1159/000093206. Epub 2006 May 8.
Nasal polyposis is mostly associated with eosinophilia of mucosal tissue. This points to the implication of CC chemokines in nasal eosinophilia. Recently the CC chemokine eotaxin-2 (CCL24) was identified. This study was initiated to localize the cellular source, analyze expression of mRNA, and quantify protein synthesis of CCL24.
Specimens of nasal inferior turbinates from controls and polypous tissue from patients suffering from chronic polypous sinusitis were collected. Furthermore, fibroblasts and epithelial cells were cultured. CCL24 protein was analyzed by immunohistochemistry and ELISA, expression of mRNA by SQ-RT-PCR.
CCL24 was observed in endothelial and epithelial cells. Specimens from patients expressed significantly (>2fold) more CCL24 mRNA than controls. Fibroblasts and unstimulated cells did not express CCL24 mRNA. Upon stimulation with TNF-alpha, INF-gamma, IL-4, or costimulation with TNF-alpha and INF-gamma CCL24 mRNA was significantly enhanced (3.2-19.6%). In controls, fibroblast, and unstimulated cells CCL24 protein was below detection limit. Most polyps comprised significant amounts of CCL24 (mean 0.24 ng/mg). TNF-alpha, INF-gamma or IL-4 induced CCL24 protein (0.1-0.3 ng/ml) in epithelial cells. Costimulation with TNF-alpha and IL-4 (0.1-30 and 1-30 ng/ml, respectively) synergistically induced synthesis of CCL24 protein (0.18-0.31 ng/ml).
In nasal polyps endothelial and epithelial cells are obviously the main source of CCL24, which was shown for transcription (mRNA) and production (protein) levels and was associated with diseases. Results gave evidence of CLL24- directed migration of cells from inside (the bloodstream) to the epithelial side (mucosa) in eosinophilic inflammatory diseases, e.g. nasal polyposis.
鼻息肉病大多与黏膜组织嗜酸性粒细胞增多有关。这表明CC趋化因子与鼻嗜酸性粒细胞增多有关。最近，CC趋化因子嗜酸性粒细胞趋化因子-2（CCL24）被鉴定出来。本研究旨在定位细胞来源，分析mRNA表达，并定量CCL24的蛋白质合成。
收集对照组的鼻下鼻甲标本以及慢性鼻息肉鼻窦炎患者的息肉组织标本。此外，培养成纤维细胞和上皮细胞。通过免疫组织化学和酶联免疫吸附测定法分析CCL24蛋白，通过半定量逆转录聚合酶链反应分析mRNA表达。
在内皮细胞和上皮细胞中观察到CCL24。患者标本中CCL24 mRNA的表达明显高于对照组（>2倍）。成纤维细胞和未受刺激的细胞不表达CCL24 mRNA。在用肿瘤坏死因子-α、干扰素-γ、白细胞介素-4刺激后，或在肿瘤坏死因子-α和干扰素-γ共同刺激下，CCL24 mRNA显著增强（3.2%-19.6%）。在对照组、成纤维细胞和未受刺激的细胞中，CCL24蛋白低于检测限。大多数息肉含有大量的CCL24（平均0.24 ng/mg）。肿瘤坏死因子-α、干扰素-γ或白细胞介素-4可诱导上皮细胞产生CCL24蛋白（0.1-0.3 ng/ml）。肿瘤坏死因子-α和白细胞介素-4（分别为0.1-30和1-30 ng/ml）共同刺激可协同诱导CCL24蛋白合成（0.18-
