Association of different cell types and inflammation in early acne vulgaris.

Acne vulgaris, one of the most common skin diseases, is a chronic cutaneous inflammation of the upper pilosebaceous unit (PSU) with complex pathogenesis. Inflammation plays a central role in the pathogenesis of acne vulgaris. During the inflammatory process, the innate and adaptive immune systems are coordinately activated to induce immune responses. Understanding the infiltration and cytokine secretion of differential cells in acne lesions, especially in the early stages of inflammation, will provide an insight into the pathogenesis of acne. The purpose of this review is to synthesize the association of different cell types with inflammation in early acne vulgaris and provide a comprehensive understanding of skin inflammation and immune responses.

Bioaccumulation and trophic transfer of antibiotics in the aquatic and terrestrial food webs of the Yellow River Delta.

Antibiotic pollution caused by aquaculture industries is a common problem in the wetland of the Yellow River Delta (YRD). Aquatic and terrestrial food webs coexist and interact in wetlands. However, there are few comparative studies on antibiotics in these two food webs. This study investigated the occurrence, bioaccumulation, and trophic transfer of 19 antibiotics in the aquatic and terrestrial food webs of the YRD, and discussed the effects of physicochemical parameters in different food webs. The total concentrations of antibiotics in aquatic organisms and terrestrial organisms ranged from 11.61 to 63.08 ng/g dry weight (dw) and 4.21-9.11 ng/g dw, respectively. BAF (bioaccumulation factor), BSAFa (biota sediment accumulation factor), and BSAFt (biota soil accumulation factor) were used to explore the bioaccumulation capacity of antibiotics. The calculation results of these three factors showed that fluoroquinolones (FQs) had the highest bioaccumulation capacity. As for the trophic transfer, the total concentrations of antibiotics were biodiluted in the aquatic food web while biomagnified in the terrestrial food web. Physicochemical parameters of the antibiotics showed that log Kow (octanol-water partition coefficient)/log Dow (pH-dependent distribution coefficient) and log Koa (octanol-air partition coefficient) were good predictors for antibiotic bioaccumulation in the aquatic and terrestrial organisms of the YRD, respectively. In addition, the increasing log Dow and log Koa led to a rise of TMF (trophic magnification factor) in the aquatic food web while a decrease of TMF in the terrestrial food web. Overall, these results provide insights into the mechanisms on bioaccumulation and trophic transfer of antibiotics in different food webs.

Knockdown of H19 Inhibits the Pathogenesis of Acne Vulgaris by Targeting the miR-196a/TLR2/NF-κB Axis.

Acne vulgaris (AV) is a chronic inflammatory disease of the pilosebaceous unit, and Propionibacterium acnes (P. acnes) has been implicated in acne inflammation. Numerous studies have shown that non-coding RNAs play important roles in regulating the pathophysiological processes of acne. In addition, the first imprinted long non-coding RNA (lncRNA) identified, H19, plays a critical role in inflammatory disease. However, the expression and role of H19 in AV remain unclear. In this study, we investigated the effects of H19 in keratinocytes and explored the regulatory mechanisms underlying these effects. H19 was upregulated in keratinocytes treated with P. acnes in a concentration-dependent manner. The phosphorylated forms of the nuclear factor (NF)-κB-related proteins IκBα (p-IκBα) and p65 (p-P65) were significantly upregulated after P. acnes treatment. Additionally, secretion of the proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 was upregulated in a concentration-dependent manner. Knockdown of H19 inhibited the expression of p-IκBα and p-P65 as well as the secretion of TNF-α, IL-6, and IL-8 in keratinocytes treated with P. acnes. Moreover, H19 was found to exert its proinflammatory effects by activating NF-κB. H19, which was localized mainly in the cytoplasm of keratinocytes, facilitated Toll-like receptor 2 (TLR2) expression by acting as a miR-196a sponge. H19 thus promoted the activation of NF-κB and the secretion of inflammatory cytokines through the miR-196a/TLR2 axis. These findings provide novel insight into the pathogenesis of AV.