High mobility group box-1 (HMGB1) has been implicated as a pro-inflammatory cytokine in the pathogenesis of various inflammatory and autoimmune diseases. However, information about HMGB1 in inflammatory skin diseases is unknown. Herein, we investigated the serum HMGB1 levels and tissue HMGB1 expression in patients with psoriasis vulgaris (PV) and atopic dermatitis (AD). Serum levels of HMGB1 in patients with PV and AD were detected by enzyme-linked immunosorbent assay (ELISA). The expression of HMGB1 in lesional skin was evaluated by immunohistochemistry and immunofluorescence. Protein levels of HMGB1 in the nuclear fraction and cytoplasmic fraction were determined by western blot. Serum levels of HMGB1 in patients with PV but not AD were significantly higher than those in nornal controls. Moreover, serum HMGB1 levels were correlated with the severity of PV according to PASI socres. Furthermore, by immunohistochemistry and immunofluorescence, we showed that the expression of HMGB1 in normal skin was almost completely restricted to the nucleus. However, abundant cytoplasmic expression of HMGB1 was observed in the epidermis in lesional skin of PV patients. In addition, western blot data indicated that HMGB1 expression was in the nucleus protein and was absent in the cytoplasm protein in control group. In contrast, HMGB1 expression in the cytoplasmic fraction was detectable in AD patients and more distinct in PV patients. Taken together, this study provides first observations on the association of HMGB1 with PV, and showed the elevated HMGB1 serum levels and altered HMGB1 distribution in lesional skin in patients with PV. We suggest that HMGB1 might be involved in the pathogenesis of PV.
With the improvement of living standards and dietary changes, childhood obesity has increased worldwide. This study aimed to understand the differences of intestinal flora structure between obese and normal children at school-age. Using the next generation sequencing platform, Illumina Miseq, 16S rDNA high-throughput sequencing technology, we analyzed the diversity and relative abundance of intestinal flora in 39 obese and 38 normal control school-age children. First, we categorized gut bacteria on the basis of their Operational taxonomic units (OTUs) using the RDP 16s rRNA database in RDP classifier. The alpha (α) diversity was used to measure the diversity within a sample and is calculated as a value for each sample. The beta (β) diversity was used to compare different samples and to measure the dissimilarity between each other sample. Our results indicated that intestinal flora in obese children showed lower diversity than normal controls. Significant differences of relative abundance of intestinal flora were detected at multiple levels of classifications. Identification of intestinal flora with significant difference between obese and normal children may provide important information to uncover the roles of these specific bacteria in the development of obesity and find new strategy to prevent and treat obesity through intervening the intestinal flora.
BackgroundTo determine the correlation between obesity in school-aged children and imbalance of gut microbes by examining the ratio change of intestinal Bifidobacteria and E.coli in obese children compared to non-obese controls.MethodsA hospital-based 1:1 case–control study was performed. Fecal samples of the subjects were collected for DNA extraction and analyzed by quantitative real-time PCR (qPCR) to determine the copy number of Bifidobacteria and E.coli. The ratio of two microbes (B/E) was then calculated and statistically analyzed.ResultsSubjects of the obesity group and control group showed no significant difference in age, gender or height (P > 0.05); whereas they had significant differences in body weight and BMI. Copy numbers of Bifidobacteria and E.coli per gram of wet fecal samples were first determined using qPCR in both obese and normal groups, which were further used for the calculation of B/E ratio. We found that B/E ration in the two groups showed significant difference (P < 0.05). Corrected χ2 test was performed for the two groups against B/E < 1, and it was found that there was a positive correlation (OR = 719.2, OR 95% C.I. = 81.57-6341.18) between B/E ratio decrease with childhood obesity.ConclusionsThe obese children have a lower amount of Bifidobacteria and higher amount of E.coli (smaller B/E ratio) compared to normal non-obese children. It was suggested that obesity in children may be associated with the imbalance of gut microbes.
Peoniflorin (PF) extracted from the root of Paeonia lactiflora pall displays anti-inflammation and antioxidant properties in several animal models. Chemokines are vital for directing the movement of circulating leukocytes to the sites of inflammation and are involved in the pathogenesis of various inflammatory skin diseases. Herein, we investigated the effects and potential mechanisms of PF on tumor necrosis factor-α (TNF-α) induced chemokine production in human dermal microvascular endothelial cells. Human dermal microvascular endothelial cell line (HMEC-1) was treated by TNF-α with or without PF. PF markedly attenuated TNF-α-induced chemokines (including CCL2, CCL5, CCL20, CXCL8, CXCL16 and CX3CL1) mRNA expression in HMEC-1. PF also reduced the secretion of these chemokines in culture supernatants. In addition, endothelial activation in the presence of PF markedly blocked the chemotactic activities of TNF-α-stimulated HMEC-1 supernatant on promyelocytic leukemia cell line (HL-60) or the acute mature monocytic leukemia cell line (THP-1) cell migration. Furthermore, Western blot data revealed TNF-α upregulated phosphorylation of inhibitor of κB-α (IκBα) and phosphorylation of extracellular signal-regulated kinase (ERK)1/2, which was almost completely reversed by PF. Finally, PF inhibited nuclear factor-κB (NF-κB) nuclear translocation to the nucleus. Taken together, our data provide the first evidence that PF has an anti-inflammatory ability against TNF-α-induced chemokine production and leukocyte migration, which may be at least partly related to the inhibition of NF-κB and ERK pathway. PF may be a candidate medicine for the treatment of inflammatory skin diseases.
Our previous work indicated that TWEAK is associated with various types of cutaneous vasculitis (CV). Herein, we investigate the effects of TWEAK on vascular injury and adhesion molecule expression in CV mice. We showed that TWEAK priming in mice induced a local CV. Furthermore, TWEAK priming also increased the extravasation of FITC-BSA, myeloperoxidase activity and the expression of E-selectin and ICAM-1. Conversely, TWEAK blockade ameliorated the LPS-induced vascular damage, leukocyte infiltrates and adhesion molecules expression in LPS-induced CV. In addition, TWEAK treatment of HDMECs up-regulated E-selectin and ICAM-1 expression at both mRNA and protein levels. TWEAK also enhanced the adhesion of PMNs to HDMECs. Finally, western blot data revealed that TWEAK can induce phosphorylation of p38, JNK and ERK in HDMECs. These data suggest that TWEAK acted as an inducer of E-selectin and ICAM-1 expression in CV mice and HDMECs, may contribute to the development of CV.
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