HISTAMINE-INDUCED INHIBITION OF NEUTROPHIL CHEMOTAXIS AND T-LYMPHOCYTE PROLIFERATION IN MAN
HISTAMINE-INDUCED INHIBITION OF NEUTROPHIL CHEMOTAXIS AND T-LYMPHOCYTE PROLIFERATION IN MAN
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DOI：
10.1111/j.1398-9995.1992.tb02385.x
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发表时间：
1992-12-01
期刊：
影响因子：
12.4
通讯作者：
RADERMECKER, MF
中科院分区：
文献类型：
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作者：
BURY, TB;CORHAY, JL;RADERMECKER, MF
组胺通过H-2受体抑制体外人中性粒细胞趋化性和T淋巴细胞增殖。本研究的目的是验证组胺在人体内的这些抑制作用。健康志愿者通过静脉内（1 mg）、皮下（1 mg）和吸入（2.4 mg）途径用组胺激发。在激发前和激发后不同时间采集静脉血。中性粒细胞的趋化性通过Boyden试验进行了研究，T淋巴细胞的增殖通过计数培养的单个核细胞中的H-3-胸苷掺入。放射免疫法测定血浆组胺含量。组胺输注引起短暂的全身症状以及组胺激发后4 h中性粒细胞趋化性（xBAR -26%+/- 6）和PHA脉冲T淋巴细胞增殖（xBAR -16%+/- 6）的显著降低。皮下注射组胺仅在注射后4 h引起中性粒细胞趋化性显著降低（xBAR -24%+/- 15）。组胺吸入耐受性良好，并在激发后2和4 h引起中性粒细胞趋化性（xBAR -40%+/- 15）和T淋巴细胞增殖（xBAR -27%+/- 6）的显著抑制。组胺激发总是伴随着血浆组胺的快速和短暂的上升。吸入H-2激动剂（Impromidine），但不是H-1激动剂（倍他司汀）引起中性粒细胞趋化性和T淋巴细胞增殖的减少。口服预处理与H-2拮抗剂（西咪替丁）组胺吸入前阻止组胺诱导的中性粒细胞趋化性和T淋巴细胞增殖的减少，而阿司咪唑，H-1拮抗剂，没有效果。总之，在给药后的几个小时内，外源性组胺通过H-2受体抑制中性粒细胞趋化性和T淋巴细胞增殖。这些观察结果与内源性组胺可能对人体炎症和免疫细胞产生某些调节作用的概念一致。
Histamine inhibits in vitro human neutrophil chemotaxis and T-lymphocyte proliferation via H-2 receptors. The aim of this study was to verify these inhibitory effects of histamine in man in vivo. Healthy volunteers were challenged with histamine by intravenous (I mg), subcutaneous (I mg) and inhalatory (2.4 mg) routes. Venous blood was taken before and at different times after challenge. Neutrophil chemotaxis was studied by the Boyden assay and T-lymphocyte proliferation by counting H-3-thymidine incorporation in cultured mononuclear cells. Plasma histamine was measured by radioimmunoassay. Histamine infusion caused transient systemic symptoms as well as a significant decrease of neutrophil chemotaxis (xBAR - 26 % +/- 6) and of PHA-pulsed T-lymphocyte proliferation (xBAR - 16 % +/- 6) 4 h after histamine challenge. Subcutaneous injection of histamine caused only a significant decrease of neutrophil chemotaxis (xBAR - 24 % +/- 15) 4 h after injection. Histamine inhalation was well tolerated and caused a significant depression of neutrophil chemotaxis (xBAR - 40 % +/- 15) and of T-lymphocyte proliferation (xBAR - 27 % +/- 6) 2 and 4 h after the challenge. Histamine challenges were always accompanied by a rapid and transient rise in plasma histamine. Inhalation of an H-2 agonist (impromidine) but not of an H-1 agonist (betahistine) caused a decrease of neutrophil chemotaxis and of T-lymphocyte proliferation. Oral pretreatment with an H-2 antagonist (cimetidine) before histamine inhalation prevented histamine-induced decrease of neutrophil chemotaxis and T-lymphocyte proliferation, whereas astemizole, an H-1 antagonist, had no effect. In conclusion, during the few hours following administration, exogenous histamine in man causes a depression of neutrophil chemotaxis and T-lymphocyte proliferation via H-2 receptors. These observations are consistent with the concept that endogenous histamine may exert some modulatory effects on inflammatory and immune cells in man.