5—氨基酮戊酸光动力对大鼠痤疮模型免疫功能的影响(1)
[摘要]目的：探讨5-氨基酮戊酸光动力(5-aminolevulinicacid photodynamic therapy，5-ALA-PDT)对大鼠痤疮模型局部免疫功能的影响及相关机制。方法：将痤疮丙酸杆菌接种大鼠耳部，建立大鼠痤疮炎症模型，给予5-ALA-PDT治疗。对组织进行HE染色，采用免疫组化法检测大鼠巨噬细胞CD68、CD163、Toll样受体2(Toll-like receptor-2，TLR2)、髓样分化因子88(MyD88)的表达。结果：痤疮丙酸杆菌接种于大鼠耳部可建立大鼠痤疮炎症模型，HE染色见大量炎性细胞弥漫性浸润。CD68、CD163、TLR2、MyD88在大鼠耳部皮肤炎症细胞质内表达，空白组较少，接种P.acnes后表达增高，加激动剂Pam3CSK4后表达更高，5-ALA-PDT治疗后较P.acnes组低。结论：大鼠耳部毛囊皮脂腺及周围可少量表达TLR2，接种痤疮丙酸杆菌后，表达显著增加，导致巨噬细胞等免疫细胞向毛囊皮脂腺周围聚集。5-ALA-PDT治疗后TLR2表达减少，减弱机体对细菌的免疫反应，从而减轻炎症。
, 百拇医药
[关键词]5-氨基酮戊酸；光动力；痤疮丙酸杆菌；痤疮；CD68；CD163；TLR2；MyD88
[中图分类号]R758.73+3 [文献标志码]A [文章编号]1008-6455(2018)06-0051-04
Abstract： Objective To study the influence of 5-ALA-PDT on the Toll-like receptor-mediated immune response in acne model in SD rats. Methods Acne inflammation model of rat ear induced by Propionibacterium acnes were established and then treated with 5-ALA-PDT. Section was made for HE staining. Immunohistochemical staining was used to observe the expression of CD68， CD163， TLR2， and MyD88. Results Acne inflammation model of rat ear was established by inoculating Propionibacterium acnes to rat ears. Diffuse infiltrations of inflammatory cell were observed by HE staining. Compared with the blank group， the expression of CD68， CD163， TLR2， MyD88 were decreased in rat ears inflammatory cells， but increased after stimulated with P.acnes and increased further after Pam3CSK4 adminstration. The expression level decreased and was lower than the model group after received 5-ALA-PDT. Conclusion TLR2 expression was low in rat ear pilosebaceous unit and its surrounding tissue and the expression increased significantly after inoculating Propionibacterium acnes， which induced macrophage infitration in pilosebaceous unit. 5-ALA-PDT decreased the expression of TLR2 and alleviates body’s immune response to bacteria， thus relieved inflammation
, 百拇医药
Key words： 5-aminolevulinic acid； photodynamic therapy； Propionibacterium acnes； acne vulgaris； CD68； CD163； TLR2； MyD88
痤瘡病变第一步为以毛囊皮脂腺单位的亚临床微粉刺，可能演变成封闭或开放粉刺和炎性病变，如丘疹、脓疱、结节和囊肿。粉刺形成被认为是涉及到毛囊的角化过度，继发于毛囊滤泡角质形成细胞过度角化以及它们脱屑减少。炎性细胞因子IL-1参与此过程，并诱导角化过度。微粉刺或粉刺后来可能发展成炎症病变，结果CD4+T细胞活化和迁移，角质形成细胞分泌细胞因子以及巨噬细胞和嗜中性粒细胞聚集到毛囊、皮脂腺，增强皮脂分泌[1]。其中，导致痤疮的发病因素主要是痤疮丙酸杆菌，是正常皮肤菌群的一部分，但它在痤疮患者的毛囊皮脂腺内明显增加[2]。痤疮丙酸杆菌通过诱导单核细胞分泌促炎症细胞因子包括TNF-α、IL-1和IL-8导致炎症发生，特别是IL-8以及其它痤疮丙酸杆菌诱导的趋化因子可召集嗜中性粒细胞到毛囊皮脂腺中发挥重要作用。此外，痤疮丙酸杆菌释放的脂肪酶、蛋白酶和透明质酸酶可导致组织损伤[3]。然而，这种细菌在痤疮的发病机制中的确切作用仍需进一步阐明。
1 材料和方法
1.1 菌液的制备：挑取单个痤疮丙酸杆菌(ATCC6919，广东微生物研究所)的菌落，并接种于厌氧脑心浸液肉汤培养基(青岛海博生物技术有限公司)中，在37℃厌氧环境下培养3d，用麦氏比浊法计数，以生理盐水调配细菌浓度至1×108cells/ml。, 百拇医药(陈向齐 宋洪涛 陈胜平)
, 百拇医药
[关键词]5-氨基酮戊酸；光动力；痤疮丙酸杆菌；痤疮；CD68；CD163；TLR2；MyD88
[中图分类号]R758.73+3 [文献标志码]A [文章编号]1008-6455(2018)06-0051-04
Abstract： Objective To study the influence of 5-ALA-PDT on the Toll-like receptor-mediated immune response in acne model in SD rats. Methods Acne inflammation model of rat ear induced by Propionibacterium acnes were established and then treated with 5-ALA-PDT. Section was made for HE staining. Immunohistochemical staining was used to observe the expression of CD68， CD163， TLR2， and MyD88. Results Acne inflammation model of rat ear was established by inoculating Propionibacterium acnes to rat ears. Diffuse infiltrations of inflammatory cell were observed by HE staining. Compared with the blank group， the expression of CD68， CD163， TLR2， MyD88 were decreased in rat ears inflammatory cells， but increased after stimulated with P.acnes and increased further after Pam3CSK4 adminstration. The expression level decreased and was lower than the model group after received 5-ALA-PDT. Conclusion TLR2 expression was low in rat ear pilosebaceous unit and its surrounding tissue and the expression increased significantly after inoculating Propionibacterium acnes， which induced macrophage infitration in pilosebaceous unit. 5-ALA-PDT decreased the expression of TLR2 and alleviates body’s immune response to bacteria， thus relieved inflammation
, 百拇医药
Key words： 5-aminolevulinic acid； photodynamic therapy； Propionibacterium acnes； acne vulgaris； CD68； CD163； TLR2； MyD88
痤瘡病变第一步为以毛囊皮脂腺单位的亚临床微粉刺，可能演变成封闭或开放粉刺和炎性病变，如丘疹、脓疱、结节和囊肿。粉刺形成被认为是涉及到毛囊的角化过度，继发于毛囊滤泡角质形成细胞过度角化以及它们脱屑减少。炎性细胞因子IL-1参与此过程，并诱导角化过度。微粉刺或粉刺后来可能发展成炎症病变，结果CD4+T细胞活化和迁移，角质形成细胞分泌细胞因子以及巨噬细胞和嗜中性粒细胞聚集到毛囊、皮脂腺，增强皮脂分泌[1]。其中，导致痤疮的发病因素主要是痤疮丙酸杆菌，是正常皮肤菌群的一部分，但它在痤疮患者的毛囊皮脂腺内明显增加[2]。痤疮丙酸杆菌通过诱导单核细胞分泌促炎症细胞因子包括TNF-α、IL-1和IL-8导致炎症发生，特别是IL-8以及其它痤疮丙酸杆菌诱导的趋化因子可召集嗜中性粒细胞到毛囊皮脂腺中发挥重要作用。此外，痤疮丙酸杆菌释放的脂肪酶、蛋白酶和透明质酸酶可导致组织损伤[3]。然而，这种细菌在痤疮的发病机制中的确切作用仍需进一步阐明。
1 材料和方法
1.1 菌液的制备：挑取单个痤疮丙酸杆菌(ATCC6919，广东微生物研究所)的菌落，并接种于厌氧脑心浸液肉汤培养基(青岛海博生物技术有限公司)中，在37℃厌氧环境下培养3d，用麦氏比浊法计数，以生理盐水调配细菌浓度至1×108cells/ml。, 百拇医药(陈向齐 宋洪涛 陈胜平)
参见：首页 > 医疗版 > 疾病专题 > 皮肤科 > 皮肤附属器官疾病 > 痤疮(青春痘)