Kriegova E, Tsyrulnyk A, Arakelyan A, Mrazek F, Ordeltova M, Petzmann S, Zatloukal J, Kolek V, du Bois R M, Popper H, Petrek M
Department of Immunology, Palacky University and Faculty Hospital Olomouc, I.P. Pavlova str. 6, 775 20, Olomouc, Czech Republic.
Inflamm Res. 2006 Oct;55(10):441-5. doi: 10.1007/s00011-006-6019-9.
CCX CKR is a decoy chemokine receptor that specifically binds the chemokines CCL19, CCL25 and CCL21. CCL19 was previously found to be upregulated in pulmonary sarcoidosis. We have, therefore, investigated CCX CKR expression in this inflammatory disease.
CCX CKR mRNA was semiquantitated using RT-PCR in unseparated bronchoalveolar (BAL) cells from sarcoidosis patients (S, n = 29) and healthy control subjects (C, n = 9). CCX CKR transcripts were upregulated in patients (mean +/- SEM); S, 0.82 +/- 0.10; C, 0.44 +/- 0.04; p = 0.01; this upregulation paralleled the disease course as assessed by the chest radiographic stage (p < 0.02). Immunocytochemistry localised the CCX CKR protein to ciliated bronchial cells. Flow cytometric fluorescent ligand uptake assay showed that these cells are able to internalize its ligand.
These observations implicate CCX CKR in the modulation of the inflammatory response in sarcoidosis.
CCX CKR是一种诱饵趋化因子受体,可特异性结合趋化因子CCL19、CCL25和CCL21。先前发现CCL19在肺结节病中上调。因此,我们研究了CCX CKR在这种炎症性疾病中的表达。
利用逆转录聚合酶链反应(RT-PCR)对结节病患者(S组,n = 29)和健康对照者(C组,n = 9)未分离的支气管肺泡(BAL)细胞中的CCX CKR mRNA进行半定量分析。患者的CCX CKR转录本上调(平均值±标准误);S组为0.82±0.10;C组为0.44±0.04;p = 0.01;这种上调与胸部X线分期评估的疾病进程平行(p < 0.02)。免疫细胞化学将CCX CKR蛋白定位到纤毛支气管细胞。流式细胞术荧光配体摄取试验表明这些细胞能够内化其配体。
这些观察结果表明CCX CKR参与了结节病炎症反应的调节。