Circulating monocytes from healthy individuals and COPD patients
Circulating monocytes from healthy individuals and COPD patients
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DOI：
10.1186/1465-9921-4-11
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发表时间：
2003-09-22
影响因子：
5.8
通讯作者：
Janciauskiene, S
中科院分区：
文献类型：
--
作者：
Aldonyte, R;Jansson, L;Janciauskiene, S
背景：慢性阻塞性肺疾病(COPD)是以单核/巨噬细胞为主的炎症相关的不完全可逆气流阻塞为特征的疾病。已知的唯一与COPD相关的遗传因素是丝氨酸酶抑制剂α1抗胰蛋白酶(AAT)的遗传性PIZ缺陷。方法：我们研究了年龄和性别匹配的健康人(n=30)和COPD(n=20)AAT缺陷者外周血单核细胞基础和脂多糖刺激下促炎分子的释放。结果：细胞培养18h后，COPD患者单核细胞释放的基质金属蛋白酶-9是对照组的2.5倍，p<；0.02，而IL-8的释放是对照组的1.8倍(p<；0.01)。与对照组相比，脂多糖刺激COPD患者单核细胞释放IL-6和MCP-1更多，而激活对照细胞则导致ICAM-1和MMP-9分泌增加。与疾病状态无关，携带PIZZ AAT携带者的单核细胞释放的TNFα较少(增加2.3倍，p<；0.03)。结论：健康受试者和COPD受试者外周血单核细胞分泌的基础致炎分子和内毒素刺激的致炎分子不同。这些发现可能对进一步研究COPD中炎性细胞募集和激活的机制有价值。
Background: Chronic obstructive pulmonary disease (COPD) is characterized by incompletely reversible airflow obstruction associated with inflammation in which monocytes/macrophages are the predominant inflammatory cells. The only known genetic factor related to COPD is inherited PiZZ deficiency of alpha1-antitrypsin (AAT), an inhibitor of serine proteases.Methods: We investigated the basal and LPS-stimulated release of pro-inflammatory molecules from blood monocytes isolated from age and gender matched healthy (n = 30) and COPD (n = 20) individuals with and without AAT deficiency.Results: After 18 h of cell culture the basal release of MMP-9 was 2.5-fold, p < 0.02 greater, whereas IL-8 was 1.8-fold (p < 0.01) lower from COPD patient monocytes than from controls. LPS-stimulated release of IL-6 and MCP-1 was greater from COPD patient's monocytes relative to controls, while activation of control cells resulted in enhanced secretion of ICAM-1 and MMP-9 compared to COPD patients. Independent of disease status, monocytes from PiZZ AAT carriers released less TNFalpha (by 2.3-fold, p < 0.03).Conclusions: The basal and LPS-stimulated secretion of specific pro-inflammatory molecules from circulating monocytes differs between healthy and COPD subjects. These findings may be valuable for further studies on the mechanisms involved in recruitment and activation of inflammatory cells in COPD.