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Toll样受体2与痤疮丙酸杆菌:它们会引发寻常痤疮的初始皮损吗?

Toll-like receptor 2 and P. acnes: do they trigger initial acne vulgaris lesions?

作者信息

Bakry Ola Ahmed, Samaka Rehab Monir, Sebika Hend, Seleit Iman

出版信息

Anal Quant Cytopathol Histpathol. 2014 Apr;36(2):100-10.

Abstract

OBJECTIVE

To elucidate the role of toll-like receptor 2 (TLR2) in the pathogenesis of acne vulgaris through its immunohistochemical localization in inflammatory and noninflammatory lesions of this disease entity.

STUDY DESIGN

Using standard immunohistochemical techniques, we examined 30 acne cases (involved and noninvolved skin) and the normal skin biopsies of 30 sex- and age-matched, healthy subjects representing the control group.

RESULTS

All examined cases showed positive TLR2 expression in epidermis, pilosebaceous units and dermal inflammatory infiltrate. There were statistically significant differences between acne-involved skin and normal skin and between acne-involved and noninvolved skin regarding TLR2 expression intensity in pilosebaceous units (p < 0.001 for both) and dermal inflammatory infiltrate (p < 0.001 for both). Intense TLR2 expression was in favor of inflammatory acne lesions in pilosebaceous units (p = 0.03) and dermal inflammatory infiltrate (p < 0.05). Intense TLR2 expression was also in favor of severe acne lesions in pilosebaceous units (p = 0.0002) and dermal inflammatory infiltrate (p = 0.001).

CONCLUSION

TLR2 is involved in the pathogenesis of inflammatory and noninflammatory acne lesions. This occurs through Propionibacterium acnes-mediated activation with the resultant release of inflammatory cytokines.

摘要

目的

通过检测Toll样受体2(TLR2)在寻常痤疮炎性和非炎性皮损中的免疫组化定位,阐明其在寻常痤疮发病机制中的作用。

研究设计

采用标准免疫组化技术,我们检测了30例痤疮患者(累及皮肤和未累及皮肤)以及30例年龄和性别匹配的健康受试者的正常皮肤活检组织作为对照组。

结果

所有检测病例在表皮、毛囊皮脂腺单位和真皮炎性浸润中均显示TLR2表达阳性。在毛囊皮脂腺单位(两者均p < 0.001)和真皮炎性浸润(两者均p < 0.001)中,痤疮累及皮肤与正常皮肤之间以及痤疮累及皮肤与未累及皮肤之间TLR2表达强度存在统计学显著差异。TLR2的高表达有利于毛囊皮脂腺单位(p = 0.03)和真皮炎性浸润(p < 0.05)中的炎性痤疮皮损。TLR2的高表达也有利于毛囊皮脂腺单位(p = 0.0002)和真皮炎性浸润(p = 0.001)中的重度痤疮皮损。

结论

TLR2参与炎性和非炎性痤疮皮损的发病机制。这是通过痤疮丙酸杆菌介导的激活以及随后炎性细胞因子的释放而发生的。

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