Abstract
Propionibacterium acnes is a commensal bacterium, which is involved in acne inflammation. An antimicrobial peptide named CEN1HC-Br, which was isolated and characterized form the green sea urchin, has been shown to possess broad-spectrum antibacterial activity. Little is known concerning the potential effects of its antibacterial and anti-inflammatory properties against P. acnes. To examine the potency of CEN1HC-Br in acne treatment, we conducted experiments to analyze the antibacterial and anti-inflammatory activities of CEN1HC-Br both in vitro and in vivo. The antimicrobial activity of CEN1HC-Br was evaluated by minimal inhibitory concentration (MIC) assays using the broth dilution method. To elucidate the in vitro anti-inflammatory effect, HaCaT cells and human monocytes were treated with different concentration of CEN1HC-Br after stimulation by P. acnes. The expression of TLR2 and the secretion of the pro-inflammatory cytokines IL-6, IL-8, IL-1β, TNF-α, IL-12, respectively, were measured by enzyme immunoassays. An evaluation of P. acnes-induced ear edema in rat ear was conducted to compare the in vivo antibacterial and anti-inflammatory effect of CEN1HC-Br, the expression of IL-8, TNF-α, MMP-2 and TLR2 was evaluated by immunohistochemistry and real time-PCR. CEN1HC-Br showed stronger antimicrobial activity against P. acnes than clindamycin. CEN1HC-Br significantly reduced the expression of interleukin IL-12p40, IL-6, IL-1β, TNF-α and TLR2 in monocytes, but they were not influenced by clindamycin. Both CEN1HC-Br and Clindamycin attenuated P. acnes-induced ear swelling in rat along with pro-inflammatory cytokines IL-8, TNF-α, MMP-2 and TLR2. Our data demonstrates that CEN1HC-Br is bactericidal against P. acnes and that it has an anti-inflammatory effect on monocytes. The anti-inflammatory effect may partially occur through TLR2 down-regulation, triggering an innate immune response and the inhibition of pro-inflammatory cytokines.
Highlights
Acne (Acne vulgaris) is a common dermatologic disorder
We found that CEN1HC-Br attenuated P. acnes caused tissue swelling, TLR2 expression, and cytokines expression such as IL-8, tumor necrosis factor (TNF)- α, matrix metalloproteinase (MMP)-2
CEN1HC-Br inhibited the growth of S. epidermidis ATCC 12228 at 16 mg/L, while the minimal inhibitory concentration (MIC) value of clindamycin was 64 mg/L
Summary
85% of all individuals experience acne to some degree during the adolescence. Acne can have profound psychosocial effects and may undermine self-confidence and self-esteem at a vulnerable time in life [11]. Acne is a multifactorial chronic inflammatory disease of the pilosebaceous duct, including non-inflammatory open and closed comedones and inflammatory papules, pustules, nodules, and cysts. Lesions may be present on the face, neck, chest, or back-areas with the greatest density of pilosebaceous units [4]. Acne has four main pathogenetic mechanisms: abnormal keratinocyte proliferation and desquamation that leads to ductal obstruction, androgen driven increase in sebum production, proliferation of Propionibacterium acnes, and the products of inflammation [1]. The crucial steps for control of acne are to avoid P. acne colonization and inflammation in the pilosebaceous units
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