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老年多形核细胞呼吸爆发与黏附能力之间的关系。

Relationship between respiratory burst and adhesiveness capacity in elderly polymorphonuclear cells.

作者信息

Tortorella C, Ottolenghi A, Pugliese P, Jirillo E, Antonaci S

机构信息

Medicina Interna, Istituto di Medicina Clinica, University of Bari Medical Faculty, Italy.

出版信息

Mech Ageing Dev. 1993 Jun;69(1-2):53-63. doi: 10.1016/0047-6374(93)90071-x.

DOI:10.1016/0047-6374(93)90071-x
PMID:8397329
Abstract

Polymorphonuclear cell (PMN) activation was assessed in 30 aged donors, in terms of either adherence to different substrates or superoxide anion (O2-) generation by adhering and suspended cells in response to several agonists. Results showed that PMN in suspension from elderly individuals displayed a phorbol 12-myristate 13-acetate (PMA)-triggered O2- responsiveness which overlapped that seen in the younger counterpart, while a significant decrease of respiratory burst was observed in the presence of formyl-methionyl-leucine-phenylalanine (FMLP). Moreover, in spite of a normal nylon fiber adhesiveness, aged individuals exhibited a reduced PMN adherence to foetal calf serum (FCS)-coated plastic surfaces by using either PMA or FMLP as stimulant. However, elderly adhering cells produced higher amounts of O2- than homologous neutrophils in suspension. Cell pretreatment with anti-CD11b, anti-CD11c and anti-CD18 antibodies led to a further inhibition of PMN adhesion to FCS-coated plates. By contrast, under the same experimental conditions, O2- generation from adhering cells was reduced by using anti-CD18 antibody only. Altogether, these findings provide additional evidence for an imbalance of PMN-mediated functions in the elderly.

摘要

在30名老年供体中评估了多形核细胞(PMN)的活化情况,评估内容包括PMN对不同底物的黏附情况,以及黏附细胞和悬浮细胞对几种激动剂产生超氧阴离子(O2-)的情况。结果显示,老年个体悬浮的PMN对佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)触发的O2-反应性与年轻个体相似,而在存在甲酰甲硫氨酰亮氨酰苯丙氨酸(FMLP)的情况下,呼吸爆发显著降低。此外,尽管老年个体的PMN对尼龙纤维的黏附性正常,但以PMA或FMLP作为刺激物时,其PMN对胎牛血清(FCS)包被的塑料表面的黏附性降低。然而,老年黏附细胞产生的O2-比悬浮的同源中性粒细胞更多。用抗CD11b、抗CD11c和抗CD18抗体对细胞进行预处理会进一步抑制PMN对FCS包被平板的黏附。相比之下,在相同实验条件下,仅使用抗CD18抗体可降低黏附细胞产生O2-的能力。总之,这些发现为老年人PMN介导的功能失衡提供了更多证据。

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