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青少年牙周炎患者游离胞浆钙变化及中性粒细胞趋化性的改变

Altered free cytosolic calcium changes and neutrophil chemotaxis in patients with juvenile periodontitis.

作者信息

Agarwal S, Reynolds M A, Duckett L D, Suzuki J B

出版信息

J Periodontal Res. 1989 Mar;24(2):149-54. doi: 10.1111/j.1600-0765.1989.tb00870.x.

Abstract

Nearly 70-75% of patients with localized juvenile periodontitis (JP) have abnormal polymorphonuclear leukocytic (PMN) chemotaxis. The objective of this study was to determine whether the lower chemotactic response in PMNs from JP patients is associated with a defect in intracellular signal transduction, as measured by stimulus-induced changes in free cytosolic calcium (Ca2+) mobilization. We report that peptide chemoattractants such as N-formyl-methionyl-leucyl-phenylalanine (fMLP) and the complement fragment C5a in direct comparative studies induced lower amounts of initial Ca2+ mobilization in PMNs from JP patients than healthy controls, as monitored by intracellular fura-2 fluorescence. The initial resting levels of free cytosolic Ca2+ in PMNs from JP patients and normal individuals were found to be similar. fMLP and C5a both mobilized Ca2+ in PMNs in a dose-dependent manner. Treatment of PMNs from 0.16 to 20 nM fMLP and 0.2 to 20 nM C5a resulted in elevated levels of free cytosolic Ca2+. However, above 20 nM fMLP and 5 nM C5a concentrations the extent of total Ca2+ mobilization did not differ significantly. Although fMLP and C5a caused Ca2+ mobilization in PMN cells from JP and healthy control subjects, fMLP stimulation induced higher levels of free cytosolic Ca2+ mobilization in PMN cells from healthy control subjects (141.29 +/- 25.55 nM/2 x 10(6) PMNs), than PMNs from JP patients (62.33 +/- 23.76 nM/2 x 10(6) PMNs). Similarly C5a induced higher levels of Ca2+ mobilization in PMNs from healthy control individuals (130.43 +/- 18.26 nM Ca2+/2 x 10(6) PMNs)O, when compared to JP patients (49.92 +/- 14.92 nM Ca2+/2 x 10(6) PMNs).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

近70%-75%的局限性青少年牙周炎(JP)患者存在多形核白细胞(PMN)趋化异常。本研究的目的是确定JP患者PMN中较低的趋化反应是否与细胞内信号转导缺陷有关,该缺陷通过刺激诱导的游离胞质钙(Ca2+)动员变化来衡量。我们报告,在直接比较研究中,肽趋化剂如N-甲酰甲硫氨酰亮氨酰苯丙氨酸(fMLP)和补体片段C5a在JP患者的PMN中诱导的初始Ca2+动员量低于健康对照,通过细胞内fura-2荧光监测。发现JP患者和正常个体PMN中游离胞质Ca2+的初始静息水平相似。fMLP和C5a均以剂量依赖方式在PMN中动员Ca2+。用0.16至20 nM fMLP和0.2至20 nM C5a处理PMN导致游离胞质Ca水平升高。然而,高于20 nM fMLP和5 nM C5a浓度时,总Ca2+动员程度无显著差异。尽管fMLP和C5a在JP和健康对照受试者的PMN细胞中引起Ca2+动员,但fMLP刺激在健康对照受试者的PMN细胞中诱导的游离胞质Ca2+动员水平(141.29±25.55 nM/2×10(6) PMN)高于JP患者的PMN(62.33±23.76 nM/2×10(6) PMN)。同样,与JP患者(49.92±14.92 nM Ca2+/2×10(6) PMN)相比,C5a在健康对照个体的PMN中诱导更高水平的Ca2+动员(130.43±18.2 nM Ca2+/2×10(6) PMN)。(摘要截断于250字)

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