CUTANEOUS LATE-PHASE RESPONSE TO ALLERGEN - MEDIATOR RELEASE AND INFLAMMATORY CELL INFILTRATION
CUTANEOUS LATE-PHASE RESPONSE TO ALLERGEN - MEDIATOR RELEASE AND INFLAMMATORY CELL INFILTRATION
复制标题
DOI：
10.1172/jci114047
复制
发表时间：
1989-05-01
影响因子：
15.9
通讯作者：
LICHTENSTEIN, LM
中科院分区：
文献类型：
--
作者：
CHARLESWORTH, EN;HOOD, AF;LICHTENSTEIN, LM
为了更好地定义炎症浸润和介质释放的动力学在皮肤的晚期反应（LPR），我们检查了皮肤活检8小时，和皮肤腔细胞计数和介质释放12小时后抗原的挑战。与对照部位相比，抗原刺激的活检部位含有14倍多的嗜碱性粒细胞（P < 0.01）和6倍多的嗜酸性粒细胞（P < 0.001），单核细胞（P < 0.03）和中性粒细胞（P ≤ 0.01）多1至2倍。0.01）。 在皮肤腔室中也发现了类似的变化。虽然在对照室中有中性粒细胞，但在抗原攻击部位中它们的数量仅为两倍（P < 0.01）。嗜酸性粒细胞为35倍（P <0.05）。0.03）在抗原室中比对照在8-12小时更普遍，并且嗜碱性粒细胞在第8小时开始被注意到并且是对照的20倍（P ≤ 0.05）。0.03）在接下来的4小时内在抗原室中更加浓缩。抗原和对照泡罩之间的单核细胞无显著差异。关于炎症介质，有组胺的初始峰值（13.2 ± 0.01）。2.9 ng/ml）。随后，该水平降至. apprx。2ng/ml，随后从第8小时开始第二次上升并增加至9.8 ±。2.8 ng/ml。组胺的这种继发性增加与所观察到的嗜碱性粒细胞的流入显著相关（r = 0.81，P < 0.05），水疱液中的PGD 2上升至371 ± 0.01。25 pg/ml，然后在最后4 h缓慢降至该水平的一半。因此，皮肤LPR已显示出组胺水平的继发性增加以及嗜酸性粒细胞和嗜碱性粒细胞的显著特异性增加，介质释放显然来自后者细胞。
To better define the inflammatory infiltrates and kinetics of mediator release during the cutaneous late-phase reaction (LPR), we examined skin biopsies at 8 h, and skin chamber cell counts and mediator release for 12 h after antigen challenge. Compared with the control sites, the antigen-stimulated biopsy sites contained 14 times as many basophils (P < 0.01) and six times as many eosinophils (P < 0.001) with one to two fold more mononuclear cells (P < 0.03) and neutrophils (P .ltoreq. 0.01). Similar changes were found in the skin chambers. Although there were neutrophils in the control chamber, they were only twice as numerous in the antigen challenged site (P < 0.01). Eosinophils were 35-fold (P .ltoreq. 0.03) more prevalent in the antigen chamber than the control for hours 8-12 and basophils were noted starting in the eighth hour and were 20-fold (P .ltoreq. 0.03) more concentrated in the antigen chamber during the next 4 h. The mononuclear cells were not significantly different between antigen and control blisters. With respect to inflammatory mediators, there was an initial peak of histamine (13.2 .+-. 2.9 ng/ml) in the blister fluid at 1 h. The level then fell to .apprx. 2 ng/ml, followed by a secondary rise starting to the eighth hour and increasing to 9.8 .+-. 2.8 ng/ml by the twelfth hour. This secondary increase in histamine correlated significantly (r = 0.81, P < 0.05) with the observed influx of basophils, PGD2 in the blister fluid rose to 371 .+-. 25 pg/ml during the first 4 h and then slowly decreased to half this level during the last 4 h. Thus, the cutaneous LPR has been shown to manifest a secondary increase in histamine levels and a markedly specific increase in eosinophils and basophils with mediator release apparently being derived from the latter cells.