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.

寻常痤疮（AV）是皮脂腺单位的一种慢性炎症性疾病，痤疮丙酸杆菌（P. acnes）与痤疮炎症有关。大量研究表明，非编码RNA在调节痤疮的病理生理过程中起着重要作用。另外，鉴定出的第一个印迹长非编码RNA（lncRNA）在炎症性疾病中起关键作用。但是，尚不清楚H19在AV中的表达和作用。在这项研究中，我们调查了H19在角质形成细胞中的作用，并探讨了这些作用的调控机制。H19在痤疮丙酸杆菌治疗的角质形成细胞中被上调以浓度依赖的方式。痤疮丙酸杆菌治疗后，核因子（NF）-κB相关蛋白IκBα（p-IκBα）和p65（p-P65）的磷酸化形式显着上调。另外，促炎细胞因子肿瘤坏死因子（TNF）-α，白介素（IL）-6和IL-8的分泌以浓度依赖的方式上调。敲除H19可以抑制痤疮丙酸杆菌处理后的角质形成细胞中p-IκBα和p-P65的表达以及TNF-α，IL-6和IL-8的分泌。。此外，发现H19通过激活NF-κB发挥其促炎作用。H19主要位于角质形成细胞的细胞质中，它通过充当miR-196a海绵来促进Toll样受体2（TLR2）的表达。因此，H19通过miR-196a / TLR2轴促进了NF-κB的活化和炎性细胞因子的分泌。这些发现为AV的发病机理提供了新颖的见解。