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化脓性汗腺炎中的宿主防御机制。

Host-defense mechanisms in hidradenitis suppurativa.

作者信息

Dvorak V C, Root R K, MacGregor R R

出版信息

Arch Dermatol. 1977 Apr;113(4):450-3.

PMID:848973
Abstract

Host-defense mechanisms were studied in seven patients with active hidradenitis suppurativa (HS). Granulocyte phagocytic function was measured by ingestion of Staphylococcus aureus labeled with radioactive carbon 14 and intracellular killing was determined by bactericidal pour plate method. Chemotaxis was measured by radioactive counting of sodium chromate Cr 51 granulocytes migrating in modified Boyden chambers. Granulocyte adherence was estimated in vitro by filtering blood samples through nylon fiber columns. Cell-mediated immunity was measured by intradermal delayed hypersensitivity responses to Candida, mumps. streptokinase/streptodornase, and purified protein derivative antigens. No abnormality was demonstrated in any granulocyte or cell-mediated immune function tests. Moreover, all patients had normal immunoglobulin levels and elevated total hemolytic complement. Therefore, we conclude that HS is a localized chronic infection of apocrine glands without a generalized defect in host defense.

摘要

对7例活动期化脓性汗腺炎(HS)患者的宿主防御机制进行了研究。通过摄取用放射性碳14标记的金黄色葡萄球菌来测量粒细胞吞噬功能,并通过杀菌倾注平板法测定细胞内杀伤能力。趋化性通过对在改良博伊登小室中迁移的铬51酸钠粒细胞进行放射性计数来测量。通过尼龙纤维柱过滤血样在体外评估粒细胞黏附情况。通过对念珠菌、腮腺炎、链激酶/链道酶和纯化蛋白衍生物抗原的皮内迟发型超敏反应来测量细胞介导的免疫。在任何粒细胞或细胞介导的免疫功能测试中均未发现异常。此外,所有患者的免疫球蛋白水平正常,总溶血补体升高。因此,我们得出结论,HS是顶泌汗腺的局限性慢性感染,宿主防御无全身性缺陷。

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