3.8 Article

Modulation of Toll Like Receptor-2 on sebaceous gland by the treatment of adult female acne

期刊

DERMATO-ENDOCRINOLOGY
卷 9, 期 1, 页码 -

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/19381980.2017.1361570

关键词

Acne; toll-like receptor 2; combined oral contraceptive; azelaic acid; sebaceous glands

资金

  1. Dermatology - Sao Paulo Regional of Brazilian
  2. Society of Dermatology - FUNADERSP

向作者/读者索取更多资源

Adult female acne is a chronic inflammatory, immune-mediated disease that affects the pilosebaceous unit in women in their 20s to 40s, and is considered different from acne vulgaris. Propionibacterium acnes is recognized by TLR-2, resulting in activation of this receptor and an inflammatory response through the NF kappa B pathway. This therapeutic, interventional, open, randomized, evaluator-blinded and comparative trial included 38 adult women with moderate facial acne and 10 age-matched controls, all aged between 26 and 44 years. Two treatments were performed over six months: 15% azelaic acid gel (AA) bid (n = 18) and oral contraceptive (COC) drospirenone 3 mg/ethinylestradiol .02 mg (n = 20). Biopsies were taken at baseline (control, lesion, perilesional) and at the conclusion (lesion and perilesional) of the study to evaluate TLR-2 expression by immunohistochemistry. Lesion count and blind photographic evaluation were used for efficacy. The groups were homogeneous: 70% of lesions were located in the submandibular area, 95% of participants had inflammatory lesions; of these, 50% had persistent and 50% had late-onset acne. The mean ages were 33.7 +/- 5.5 and 33.1 +/- 5.3 years (COC and AA group, respectively). A moderate clinical improvement was observed in both groups. No difference in TLR-2 expression in the lesion or perilesional areas was observed; however, reduced TLR-2 expression was seen in the control group. A significant reduction in expression was observed after both treatments, with no difference between the groups. This finding suggests an anti-inflammatory effect of COCs and AA in adult female acne, via modulation of the TLR-2 receptor.

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