Colditz I G
CSIRO, Division of Animal Health, Armidale, N.S.W.
Inflammation. 1988 Jun;12(3):251-63. doi: 10.1007/BF00920077.
A model of acute inflammation in the skin of sheep was developed using [111In]oxine-labeled neutrophils to quantify the accumulation of neutrophils in inflammatory lesions. Peak accumulation occurred during the first hour in lesions induced by zymosan-activated sheep plasma (ZAP, 100%) and during the second hour in lesions induced by endotoxin (10(-11) moles) and casein (2 x 10(-8) moles). The accumulation of neutrophils after the final stimulus diminished when lesions were restimulated every 2 h on two or more occasions. Thus desensitization of inflammatory lesions previously observed in rabbit skin is not restricted to that species. The early accumulation of neutrophils in primary and restimulated lesions was measured in lesions from 10 min to 2 h old. In primary lesions, ZAP induced significant neutrophil accumulation by 10 min, whereas 30 to 45 min elapsed before significant neutrophil accumulation occurred in lesions induced with endotoxin and casein. The initial responses in restimulated lesions were not diminished, but there was a failure of neutrophil accumulation to continue for as long as occurred in primary lesions. This finding indicates that regulation of the neutrophil influx into dermal inflammatory lesions may occur at a point after occupancy of the putative tissue receptors in the pathway which leads to accumulation of neutrophils at the injection site. The results indicate that there are at least two patterns of neutrophil accumulation in primary inflammatory lesions. The delayed pattern of neutrophil accumulation induced by casein and endotoxin resembles the enhanced binding of neutrophils to stimulated endothelial cultures in vitro, whereas the basis for the immediate response induced by ZAP remains conjectural. It is proposed that the primary action of chemotactic agents may be to provoke changes in the adhesive properties of endothelium and resident connective tissue cells thus permitting the migration of neutrophils into inflammatory lesions.
利用[111铟]氧嗪标记的中性粒细胞建立了绵羊皮肤急性炎症模型，以量化中性粒细胞在炎症病变中的积聚情况。在由酵母聚糖激活的绵羊血浆（ZAP，100%）诱导的病变中，峰值积聚发生在第1小时；在由内毒素（10^(-11)摩尔）和酪蛋白（2×10^(-8)摩尔）诱导的病变中，峰值积聚发生在第2小时。当每2小时对病变进行两次或更多次再刺激时，最终刺激后中性粒细胞的积聚减少。因此，先前在兔皮肤中观察到的炎症病变脱敏现象并不局限于该物种。在10分钟至2小时龄的病变中测量了原发性和再刺激病变中中性粒细胞的早期积聚情况。在原发性病变中，ZAP在10分钟时诱导了显著的中性粒细胞积聚，而在内毒素和酪蛋白诱导的病变中，30至45分钟后才出现显著的中性粒细胞积聚。再刺激病变中的初始反应并未减弱，但中性粒细胞的积聚未能像原发性病变那样持续那么长时间。这一发现表明，中性粒细胞流入皮肤炎症病变的调节可能发生在导致中性粒细胞在注射部位积聚的途径中假定的组织受体被占据之后的某个点。结果表明，原发性炎症病变中至少存在两种中性粒细胞积聚模式。酪蛋白和内毒素诱导的中性粒细胞积聚延迟模式类似于体外中性粒细胞与受刺激内皮细胞培养物的增强结合，而ZAP诱导的即时反应的基础仍属推测。有人提出，趋化剂的主要作用可能是引发内皮细胞和驻留结缔组织细胞黏附特性的变化，从而使中性粒细胞能够迁移到炎症病变中。
