Abstract
Acne vulgaris is a chronic inflammatory condition of skin sebaceous follicles. To explore its effects on acne vulgaris, we investigated the antibacterial and anti-inflammatory activities of Sargassum miyabei Yendo (a brown alga) ethanolic extract (SMYEE) on Cutibacterium acnes (C. acnes)-stimulated inflammatory responses, both in vivo and in vitro. To induce inflammation in vivo, C. acnes was intradermally injected into the dorsal skin of mice, to which SMYEE was applied. The antimicrobial activity of SMYEE was evaluated by the determination of minimum inhibitory concentrations (MICs). To explore in vitro anti-inflammatory effects, HaCaT cells were stimulated with C. acnes after treatment with SMYEE. The levels of IL-8 and the underlying molecular effects in C. acnes-stimulated HaCaT cells were assessed by enzyme-linked immunosorbent assay, Western blotting, and an electrophoretic mobility shift assay. Mouse skin lesions improved after treatment with SMYEE (50 μg/mouse). Neutrophil infiltration was significantly reduced in SMYEE-treated compared to SMYEE-untreated skin lesions. SMYEE reversed the C. acnes-induced increase in IL-8 levels in HaCaT cells and suppressed dHL-60 cell migration. SMYEE also inhibited C. acnes-induced phosphorylation of the extracellular signal-regulated kinase and inhibited activator protein-1 signaling. SMYEE may be a useful treatment for C. acnes-induced acne vulgaris.
Highlights
Acne vulgaris is a skin disorder involving sebaceous follicles
The antibacterial activity of SMYEE against C. acnes strains was evaluated by the determination of minimum inhibitory concentrations (MICs) and minimum bactericidal concentrations (MBCs) (Table 1)
The MICs ranged from 128 μg/mL to 512 μg/mL and the MBCs ranged from 512 μg/mL to 4096 μg/mL
Summary
Acne vulgaris is a skin disorder involving sebaceous follicles. Cutibacterium acnes (C. acnes), a gram-positive anaerobic bacterium, triggers the inflammatory response of acne vulgaris by enhancing the secretion of interleukin-1 beta (IL-1β), IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α) by monocytic cells, because of which inflammatory lesions eventually develop [2,3]. Keratinocytes are the first-line responders of the skin’s immune system and, along with sebocytes, produce a variety of cytokines and chemokines [4]. IL-8 has been implicated in the inflammatory response of acne vulgaris [6]. P. acnes activates TLR-2 to induce the production of pro-inflammatory cytokines through activating MAP kinases (MAPKs), nuclear factor-κB (NF-κB), and activator protein (AP)-1 in facial acne lesions of patients [7]
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