ABSTRACT
Background: The etiologic factors of acne are multifactorial, including ductal epidermal hyperproliferation, excess sebum production and the presence of propionobacterium acnes [P. acnes]. Immune response to P. acnes include humoral and cell- mediated immunity as well as complement activation. The burgeoning knowledge of Toll like receptors [TLR] and its effect on innate immunity are modifying our concepts regarding comedogenesis and inflammation. Much remains to be learned about the pathogenesis of acne regarding the role of P. acnes and TLR
Objective: The aim of this work was to study the expression of TLR2, Human beta-Defensin-2 [HbetaD2] and Interleukin-8 [IL-8] in acne vulgaris patients compared to non lesional skin in order to evaluate their role in the pathogenesis of inflammatory acne
Patients and Methods: This study was conducted on 10 patients with inflammatory acne lesions. Two biopsies [from lesional and non lesional skin] were taken from each patient. Reverse transcriptionpolymerase chain reaction [RT-PCR] was conducted for the skin biopsies to detect the expression of the m-RNA of TLR-2, HbetaD-2 and IL-8
Results: The expression of the m-RNA of TLR-2, HbetaD-2 and IL-8 was statistically significantly higher in lesional skin biopsies compared with that in non lesional skin. A strong positive correlation was detected between TLR-2 and both HbetaD-2 and IL-8 in lesional skin biopsies
Conclusions: TLR-2, HbetaD-2 and IL-8 may have a role in the pathogenesis of inflammatory acne vulgaris. In acne lesions, keratinocytes express HbetaD-2 and IL-8 in response to P. acne and this is dependent on TLR-2. So, TLR-2 could be a target of therapeutic intervention to block the inflammatory cytokine response in acne patients