Groneberg D A, Bester C, Grützkau A, Serowka F, Fischer A, Henz B M, Welker P
Department of Pediatric Pneumology and Immunology, Division of Allergy Research, Charité School of Medicine, Free University and Humboldt University, Berlin, Germany.
Allergy. 2005 Jan;60(1):90-7. doi: 10.1111/j.1398-9995.2004.00628.x.
Atopic dermatitis skin lesions are characterized by inflammatory changes and epithelial hyperplasia requiring angiogenesis. As mast cells may participate in this process via bidirectional secretion of tissue-damaging enzymes and pro-angiogenic factors, the present study aimed to assess the occurrence and possible function of mast cells in the papillary dermis and in epidermal layers of atopic dermatitis lesions.
Semi-thin and serial sections in combination with immunohistochemistry, histochemistry and proliferating cell nuclear antigen (PCNA)-activity assays were used and related to epidermal thickness and targeted gene expression studies.
Mast cells were located in the papillary dermis and migrated through the basal lamina into the epidermis of atopic dermatitis lesions. An increased PCNA-activity in cells of superficial epidermal layers indicated an activation of keratinocytes and stimulation of endothelial growth. Only approximately 30% of the papillary mast cells stained with the tryptase were toluidin-blue-positive, and approximately 80% were chymase positive. A high number of mast cells expressed c-kit. Most papillary and epidermal mast cells were localized close to endothelial cells. Vascular expression of endoglin (CD105) demonstrated neoangiogenic processes. Mast cells stimulation led to the expression of proangiogenic factors. Also, gene expression of tissue-damaging factors such as matrix metalloproteinases was increased.
These data suggest that in atopic dermatitis, mast cells are abundantly localized close to and within the epidermis where they may stimulate neoangiogenesis. Via the new vessels, inflammatory cells, together with complement components and antibodies, can be transported to the epidermis to aid in the defense against environmental antigens and to maintain chronic inflammation.
特应性皮炎皮肤病变的特征是炎症变化和需要血管生成的上皮增生。由于肥大细胞可能通过双向分泌组织损伤酶和促血管生成因子参与这一过程,本研究旨在评估肥大细胞在特应性皮炎病变乳头真皮层和表皮层中的发生情况及可能的功能。
采用半薄切片和连续切片结合免疫组织化学、组织化学及增殖细胞核抗原(PCNA)活性检测,并与表皮厚度及靶向基因表达研究相关联。
肥大细胞位于乳头真皮层,并通过基膜迁移至特应性皮炎病变的表皮。表皮浅层细胞中PCNA活性增加表明角质形成细胞被激活且内皮生长受到刺激。仅约30%的用类胰蛋白酶染色的乳头肥大细胞甲苯胺蓝阳性,约80%的肥大细胞糜酶阳性。大量肥大细胞表达c-kit。大多数乳头和表皮肥大细胞定位于靠近内皮细胞处。内皮糖蛋白(CD105)的血管表达显示有新生血管形成过程。肥大细胞刺激导致促血管生成因子表达。此外,组织损伤因子如基质金属蛋白酶的基因表达也增加。
这些数据表明,在特应性皮炎中,肥大细胞大量定位于表皮附近及表皮内,在那里它们可能刺激新生血管形成。通过新血管,炎症细胞连同补体成分和抗体可被运输至表皮,以帮助抵御环境抗原并维持慢性炎症。