Rodeberg D A, Babcock G F
Shriners Burns Institute, Cincinnati, Ohio 45229-3095, USA.
Infect Immun. 1996 Jul;64(7):2812-6. doi: 10.1128/iai.64.7.2812-2816.1996.
This study investigated the role of intracellular calcium concentration ([Ca]i) as a possible intermediate in the lipopolysaccharide (LPS) second messenger pathway for the activation of neutrophils (polymorphonuclear leukocytes [PMNs]). Isolated PMNs were loaded with the calcium-sensitive fluorescent dye fura-2. The PMNs were stimulated with either LPS or the positive control formyl-Met-Leu-Phe (fMLP). As expected, PMN exposure to fMLP increased [Ca]i. However, LPS stimulation did not induce any detectable changes. Depletion of intracellular Ca stores with thapsigargin, or extracellular Ca with EGTA, significantly inhibited the upregulation of the CD11b/CD18 integrin in response to fMLP but not LPS. We conclude that [Ca]i is not an early intermediate in the second-messenger pathway for the activation of PMNs by LPS.
本研究调查了细胞内钙浓度([Ca]i)作为脂多糖(LPS)激活中性粒细胞(多形核白细胞[PMN])第二信使途径中可能的中间介质的作用。分离的PMN用钙敏荧光染料fura-2进行负载。用LPS或阳性对照甲酰甲硫氨酸亮氨酸苯丙氨酸(fMLP)刺激PMN。正如预期的那样,PMN暴露于fMLP会增加[Ca]i。然而,LPS刺激并未引起任何可检测到的变化。用毒胡萝卜素耗尽细胞内钙库,或用乙二醇双四乙酸(EGTA)耗尽细胞外钙,可显著抑制fMLP刺激引起的CD11b/CD18整合素上调,但对LPS刺激无此作用。我们得出结论,[Ca]i不是LPS激活PMN第二信使途径中的早期中间介质。