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豚鼠实验性皮肤念珠菌病中嗜碱性粒细胞积聚的可能机制研究。

Study of possible mechanisms of basophil accumulation in experimental cutaneous candidiasis in guinea pigs.

作者信息

Sohnle P G, Kirkpatrick C H

出版信息

J Allergy Clin Immunol. 1977 Feb;59(2):171-7. doi: 10.1016/0091-6749(77)90221-4.

DOI:10.1016/0091-6749(77)90221-4
PMID:833382
Abstract

It is known that certain lymphokine preparations, bacterial growth products, and factors released through complement activation have in vitro chemotactic activity for basophils. We have developed a model for acute cutaneous candidiasis in guinea pigs in which the lesions are characterized by infecting organisms in the keratin layer, early accumulation of polymorphonuclear leukocytes in the upper epidermis, and subsequent accumulation of basophils along the dermal basement membrane. The present study was undertaken to determine if any of the known chemotactic factors were operating in vivo to attract basophils. Both nonimmune guinea pigs and animals with established delayed hypersensitivity to candida had basophils in the infected skin. While immune animals showed more basophils than did nonimmune animals, the difference was not significant. Intradermal injections of a sonicate of candida or a candida growth filtrate did not cause significant accumulation of basophils. Decomplementation of the animals with cobra venom factor (CVF) did not significantly reduce the basophil numbers. Moreover, basophil accumulation occurred in animals with only minimal serum antibody to candida. These studies indicate that the basophil accumulation is due to a mechanism that is not dependent on cellular immunity, direct chemotactic activity in the candida extract, antibodies, or complement. Therefore, there may exist a previously unrecognized, nonimmunologic mechanism of chemotaxis for basophils which could possibly operate in other types of lesions and could even be involved with attraction of other types of cells.

摘要

已知某些淋巴因子制剂、细菌生长产物以及通过补体激活释放的因子在体外对嗜碱性粒细胞具有趋化活性。我们已经建立了一种豚鼠急性皮肤念珠菌病模型,其中病变的特征是角质层中有感染生物体,上表皮有多形核白细胞早期积聚,随后嗜碱性粒细胞沿真皮基底膜积聚。本研究旨在确定是否有任何已知的趋化因子在体内发挥作用以吸引嗜碱性粒细胞。未免疫的豚鼠和对念珠菌已建立迟发型超敏反应的动物在感染皮肤中均有嗜碱性粒细胞。虽然免疫动物的嗜碱性粒细胞比未免疫动物多,但差异不显著。皮内注射念珠菌超声裂解物或念珠菌生长滤液不会导致嗜碱性粒细胞显著积聚。用眼镜蛇毒因子(CVF)使动物补体灭活并没有显著减少嗜碱性粒细胞数量。此外,在仅对念珠菌有微量血清抗体的动物中也发生了嗜碱性粒细胞积聚。这些研究表明,嗜碱性粒细胞积聚是由于一种不依赖于细胞免疫、念珠菌提取物中的直接趋化活性、抗体或补体的机制。因此,可能存在一种以前未被认识的嗜碱性粒细胞趋化的非免疫机制,它可能在其他类型的病变中起作用,甚至可能与其他类型细胞的吸引有关。

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Study of possible mechanisms of basophil accumulation in experimental cutaneous candidiasis in guinea pigs.豚鼠实验性皮肤念珠菌病中嗜碱性粒细胞积聚的可能机制研究。
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Cutaneous basophil hypersensitivity and contact sensitivity after cutaneous Trichophyton mentagrophytes infection.须癣毛癣菌皮肤感染后的皮肤嗜碱性粒细胞超敏反应和接触性过敏反应。
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Participation of neutrophils and delayed hypersensitivity in the clearance of experimental cutaneous candidiasis in mice.中性粒细胞与迟发型超敏反应在小鼠实验性皮肤念珠菌病清除过程中的作用。
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