Mobilization of opioid-containing polymorphonuclear cells by hematopoietic growth factors and influence on inflammatory pain
Mobilization of opioid-containing polymorphonuclear cells by hematopoietic growth factors and influence on inflammatory pain
复制标题
DOI：
10.1097/00000542-200401000-00024
复制
发表时间：
2004-01-01
期刊：
影响因子：
8.8
通讯作者：
Stein, C
中科院分区：
文献类型：
--
作者：
Brack, A;L' Rittner, H;Stein, C
背景：在冷水游泳或局部注射促肾上腺皮质激素释放因子的刺激下，白细胞可通过分泌阿片肽，进而激活周围感觉神经元上的阿片受体来控制炎性疼痛。目的：探讨粒细胞集落刺激因子(G-CSF)和干细胞因子(SCF)联合动员多形核细胞(PMN)对弗氏完全佐剂性后足炎大鼠外周阿片类镇痛作用的影响。方法：采用放射免疫法测定G-CSF+SCF组和假手术组大鼠外周血中阿片肽含量。用流式细胞仪分析黏附分子(CD62L、CD49d、CD18)的表达、细胞在Boyden小室中的迁移和白细胞的浸润情况。光周期聚合酶链式反应定量检测趋化因子信使RNA转录。在基础状态、冷水游泳后和注射促肾上腺皮质激素释放因子后测量爪压阈值。结果：G-CSF+SCF治疗后循环PMN增加11倍(P<；0.05)。动员后的中性粒细胞中β-内啡肽含量降低，但甲硫氨酸脑啡肽含量无变化，CD62L表达下调，CD49d表达上调(但CD18无变化)，趋化因子浓度升高(P均<0.05)。4种趋化因子信使RNA中的一种在炎症反应的前2 h显著表达(P&t；0.05)，中性粒细胞和阿片类细胞的迁移率略有增加(1.5倍，P&t；0.05)，促肾上腺皮质激素释放因子和冷水游泳引起的基础爪压阈值和爪压阈值升高无明显变化(P>；0.05)。结论：G-CSF+SCF动员含阿片的中性粒细胞，但对细胞迁移和外周镇痛的影响较小，可能与趋化因子的低表达有关；在炎症的爪子和一个下降的中性粒细胞的13-内啡肽含量。
Background: Leukocytcs can control inflammatory pain by secretion of opioid peptides, stimulated by cold-water swimming or local injection of corticotropin-releasing factor, and subsequent activation of opioid receptors on peripheral sensory neurons. This study investigated whether mobilization of polymorphonuclear cells (PMN) by granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) enhances immigration of opioid-containing PMN and peripheral opioid analgesia in rats with Freund complete adjuvant-induced hind paw inflammation.Methods: In circulating PMN of rats treated with G-CSF+SCF and sham-treated rats, opioid peptide content was measured by radioinimunoassay. Expression of adhesion molecules (CD62L, CD49d, CD18), in vitro migration in the Boyden chamber, and infiltrating leukocytes were analyzed by flow cytometry. Chemokine messenger RNA transcription was quantified by Light-Cycler polymerase chain reaction. Paw pressure threshold was measured at baseline, after cold-water swimming, and after injection of corticotropin-releasing factor.Results: G-CSF+SCF treatment increased circulating PMN (11-fold, P < 0.05). Mobilized PMN had decreased content of beta-endorphin but not of Met-enkephalin per cell, down-regulation of CD62L, up-regulation of CD49d (but no change in CD18), and reduced migration toward higher chemokine concentrations (all P < 0.05). in the paw, one of four chemokine messenger RNAs was significantly expressed during the first 2 h of inflammation (P < 0.05), immigration of PMN and opioid-containing cells was slightly increased (1.5-fold, P < 0.05), and baseline paw pressure threshold, as well as paw pressure threshold increases induced by corticotropin-releasing factor and coldwater swimming, were unchanged (P > 0.05).Conclusions: G-CSF+SCF mobilized circulating opioid-containing PMN but had a minor influence on cell migration and peripheral analgesia, probably because of the low expression of chemokines; in the inflamed paw and one of the decreased 13-endorphin content in PMN.