EOSINOPENIA OF ACUTE INFECTION - PRODUCTION OF EOSINOPENIA BY CHEMOTACTIC FACTORS OF ACUTE-INFLAMMATION
EOSINOPENIA OF ACUTE INFECTION - PRODUCTION OF EOSINOPENIA BY CHEMOTACTIC FACTORS OF ACUTE-INFLAMMATION
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DOI：
10.1172/jci109789
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发表时间：
1980-01-01
影响因子：
15.9
通讯作者：
MCCALL, CE
中科院分区：
文献类型：
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作者：
BASS, DA;GONWA, TA;MCCALL, CE
急性炎症反应的一个独特方面是循环中的嗜酸性粒细胞数量迅速和持续减少，但这种嗜酸性粒细胞减少的机制尚不清楚。突发性嗜酸性粒细胞减少可能是急性炎症的少量趋化因子释放到循环中的结果。静脉注射后检测循环中嗜酸性粒细胞的数量。注射酵母多糖激活的血清，部分纯化的C5a[补体成分5的片段a]或合成肽N-甲硫基亮氨酰苯丙氨酸。这些因素中的每一个都导致循环中的嗜酸性粒细胞在1分钟内几乎消失，嗜酸性粒细胞短暂返回到.apprx。注射后10~90min达到对照水平的50%，随后下降，持续5h，外周血嗜异粒细胞数量虽有短暂下降，但在注射后6h迅速回升至高水平。这种反应不是由肾上腺调节引起的，而是在去肾上腺的兔身上正常发生的。两种变态反应性炎症趋化素，组胺和四肽缬氨酸-甘氨酸-丝氨酸-谷氨酸，没有引起明显的嗜酸性粒细胞减少。血液透析患者循环中的粒细胞激活C，表现出类似的嗜酸性粒细胞反应和中性粒细胞反应。在兔和人中，血管内激活或注射趋化因子(C5a或N-甲酰甲硫基亮氨酸苯丙氨酸)会导致短暂的非特异性粒细胞减少，随后会出现类似于急性感染时的长期嗜酸性粒细胞-中性粒细胞反应。
One distinctive aspect of the response to acute inflammation involves a rapid and persistent decrease in numbers of circulating eosinophils, yet the mechanisms of this eosinopenia are undefined. The abrupt eosinopenia may be the result of release of small amounts of the chemotactic factors of acute inflammation into the circulation. The numbers of circulating eosinophils were examined after an i.v. injection of zymosan-activated serum, partially purified C5a [fragment a of complement component 5] or the synthetic peptide, N-formylmethionylleucylphenylalanine. Each of these factors caused a virtual disappearance of circulating eosinophils within 1 min, a transient return of eosinophils to .apprx. 50% of control levels after 10-90 min and a subsequent decrease which persisted for 5 h. The numbers of circulating heterophils, although dropping transiently, rapidly returned and rose to elevated levels for 6 h after injection. The response was not caused by adrenal mediation as it occurred normally in adrenalectomized rabbits. Two chemotaxins of allergic inflammation, histamine and the tetrapeptide valine-glycine-serine-glutamic acid, did not cause significant eosinopenia. Circulating granulocytes of patients undergoing hemodialysis, which activates C, demonstrated similar eosinopenic and neutropenic-neutrophilic responses. In rabbits and in man intravascular activation or injection of chemotactic factors (C5a or N-formylmethionylleucylphenylalanine) causes brief, nonspecific granulocytopenia followed by a prolonged eosinopenic-neutrophilic response analogous to that seen during acute infection.