Pemphigus vulgaris (PV) is an autoimmune disease characterized by the production of IgG autoantibodies owing to an imbalance in the Th1/Th2 and Th17/Tregs cell pathways. The role of gut microbiota in the development of immune system and autoimmune diseases has been unraveled in the last two decades. However, data pertaining to gut microbiota of PV patients is largely lacking. We aimed to compare the gut microbiota of PV patients and healthy controls and assessed potential correlation with circulating cytokines of Th1/Th2/Th17 cell. Faecal bacterial diversity was analysed in 18 PV patients and 14 age‐ and gender‐matched healthy individuals using hypervariable tag sequencing of the V3‐V4 region of the 16S rRNA gene. Plasma levels of 20 inflammatory cytokines were assessed using the Luminex screening system. As a result, we identified 10 differentially abundant taxa between patients and controls. At the genera level, Lachnospiracea_incertae_sedis and Coprococcus decreased, while Granulicatella, Flavonifractor enriched in PV. Plasma levels of C5a, interleukin (IL)‐2R, IL‐6, IL‐8, IL‐7, IL‐1β, IL17A, IL‐5 and IL‐21 were significantly increased in PV Flavonifractor exhibited a positive correlation with C5a, IL‐6, IL‐8, IL‐7, IL‐1β, IL17A and IL‐21. Lachnospiracea_incertae_sedis and Coprococcus showed a negative correlation with IL‐17A. Our results are consistent with the hypothesis that PV patients have gut microbial dysbiosis which might contribute to the immune disorder and the development of PV.

Background: Although the changed lipid environment of the pilosebaceous unit and the growth of lipophilic Cutibacterium acnes (C. acnes) during puberty has long been considered as the trigger of acne vulgaris, the involvement of the interaction between the epidermal barrier integrity and the skin microbiome in this disease has not been fully elucidated. Objective: The aim of this study was to analyze the differences in the epidermal barrier and skin microbiota in patients with acne vulgaris and their correlation. Methods: The skin microbial samples and epidermal barrier data from 74 acne patients and 19 healthy subjects were collected in this cross-sectional study. The microbial diversity was analyzed based on a high-throughput sequencing approach that targets the V3-V4 region of the bacteria 16S ribosomal RNA genes. Results: Compared with healthy controls, acne patients had significantly increased transepidermal water loss (TEWL), pH levels, sebum, porphyrins, and red areas, and reduced skin microbiome diversity according to the goods coverage diversity index (p = 0.021), Shannon diversity index (p = 0.037), and Simpson diversity index (p = 0.023). Moreover, the diversity gradually decreased with the increase in acne grading. Based on the principal coordinate analysis (PCoA) analysis plot, the skin microbiota of acne patients and healthy controls could be divided into two different sets, which could not be used to separate acne patients with different disease severity. Finally, this study found that both TEWL and sebum were negatively associated with the Shannon and Simpson diversity index. Meanwhile, the taxa Enhydrobacter and Stenotrophomonas were positively associated with TEWL, stratum corneum hydration, respectively. Conclusion: This study demonstrated that acne vulgaris exists in patients with both damaged epithelial barriers and associated microbiota dysbiosis; the findings will help improve the understanding of the disease and may contribute to the development of better treatment options.

The tumour necrosis factor‐α (TNF‐α) promoter −308 A/G polymorphism plays an important role in the aetiology of systemic lupus erythematosus (SLE). Several studies have estimated the association between TNF‐α −308 A/G and SLE risk. However, results were inconsistent. A case–control study was carried out to explore the association between TNF‐α −308 A/G and the SLE risk in a Chinese Han population. Meta‐analysis combining present with previous studies was conducted to further explore the association. Our case–control study included 556 patients with SLE along with 570 matched healthy controls. TNF‐α −308 A allele was significantly increased in patients with SLE compared with controls (OR = 2.184, 95% CI: 1.718–2.778, P < 0.001). Genotypes AA and AG were associated with the susceptibility to SLE as compared with the GG genotype, as well as the dominant model (AA+AG versus GG), respectively. The meta‐analysis included 41 comparative studies involving 4799 patients and 6635 controls. An association between SLE and allele A was found in the overall populations (OR = 1.70, 95% CI: 1.46–1.98, P < 0.001). In addition, we discussed the correlation between this polymorphism and lupus nephritis (LN) risk, showing that allele A was significantly related to LN in the overall populations (OR = 1.80, 95% CI: 1.21–2.68, P = 0.004). The results from our case–control study and the meta‐analysis indicate that the TNF‐α −308 A allele is significantly associated with an increased risk of SLE/LN.

Objective: The aim of this research was to systematically investigate the effects of endothelial mesenchymal transition (EndMT) induced by hypoxia on the skin microvascular remodeling of systemic sclerosis (SSc) and the underlying mechanism. Methods: Skin tissues from SSc patients and controls were collected for isobaric tags for the relative and absolute quantification (iTRAQ)-based proteomics and immunohistochemical test. Human microvascular endothelial cell line-1 (HMEC-1) cultured in hypoxic or normal conditions was treated by tamoxifen or bevacizumab. Results: The iTRAQ-based proteomics indicated a significantly upregulated hypoxia-inducible factor-1 (HIF-1) signal in SSc samples. The immunohistochemical results demonstrated the significant downregulation of CD31, the positive staining of α-smooth muscle actin (α-SMA), HIF-1α, and vascular endothelial growth factor (VEGF-a) in SSc skin tissues, compared with control samples. Consistent with these observations, HMEC-1 cells cultured under hypoxic conditions exhibited a significant decrease in CD31 and VE-cadherin expression, alongside a marked increase in the expression of α-SMA and fibronectin, as well as a distinct upregulation of HIF-1α and VEGF-a, when compared with those under normal conditions. It is noteworthy that the inhibition of HIF-1α by tamoxifen effectively downregulated the hypoxic induction of VEGF-a and α-SMA while rescuing the hypoxic suppression of CD31. In addition, the VEGF-a inhibitor bevacizumab treatment had the same effect on the hypoxic expression of α-SMA and CD31, as a tamoxifen intervention, but did not reduce HIF-1α. Conclusion: These results suggest that the HIF-1α/VEGF signaling pathway can have a critical role in mediating the effect of hypoxia-induced EndMT on the skin microvascular remodeling of SSc.

Brain-derived neurotrophic factor (BDNF) is one of the proteins that contributes to the survival, growth, maintenance of neurons, and plays important roles in the pathophysiology of depression. It has been reported that depression is closely associated with the pathogenesis of acne vulgaris disease. But, there is no report of serum BDNF levels in patients with acne vulgaris. The study aimed to determine the potential association between BDNF and depressive symptoms in young adults with acne vulgaris. In this analytical cross-sectional study, the serum BDNF levels were measured in peripheral blood samples of 20 consecutive acne vulgaris patients with depression and 98 consecutive acne vulgaris patients without depression and also compared it with a 59 healthy control group by using a ELISA. The potential correlation between the BDNF levels, interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and depressive symptoms such as nine-item patient health questionnaire (PHQ-9) and Athens insomnia scale (AIS) were evaluated with multivariate logistic regression analysis. Our results showed that levels of BDNF expression were lower in consecutive acne vulgaris patients when compared with healthy control (P < 0.05). There was a negative correlation between levels of BDNF and the PHQ-9 scores (r = − 0.486, P < 0.001). Furthermore, acne vulgaris patients with depression showed lower serum BDNF levels (10.96 ± 2.12 ng/ml) compared with acne vulgaris patients without depression (13.85 ± 2.47 ng/ml), as well as with healthy control (14.35 ± 2.70 ng/mg; both P < 0.05). No difference was found in serum BDNF levels between healthy control and acne vulgaris patients without depressive symptoms (z = 0.964, P > 0.05). Similarly, the overall area under the curve of receiver operating characteristic was 0.82, indicating the highly conserving of serum BDNF levels as an biomarker for screening of depression in young adults with acne vulgaris (72% sensitivity and 85% specificity). Serum BDNF levels were decreased and negatively associated with depressive symptoms in young Chinese adults with acne vulgaris.

Several studies have reported that the tumor necrosis factor-α (TNF-α) -308G/A polymorphism is associated with susceptibility to obstructive sleep apnea-hypopnea syndrome (OSAHS). However, these results are controversial and conflicting. To evaluate the association between TNF-α-308G/A and OSAHS risk by meta-analysis. Electronic databases, including PubMed, Embase, China National Knowledge Infrastructure (CNKI), Wanfang, and Weipu, were searched to identify relevant studies. Data were extracted from the included studies. A model-free approach using odds ratio (OR), generalized odds ratio (ORG) and 95% confidence interval (CI) of the allele contrast to assess the association between the -308G/A polymorphism and OSAHS risk. Cumulative and recursive cumulative meta-analyses (CMA) were also carried out to investigate the trend and stability of effect sizes as evidence accumulated. Seven studies including 1369 OSAHS patients and 1064 controls were identified in this meta-analysis. Significant associations were derived from the variants of the allele contrast [(OR, 1.78; 95% CI, 1.45–2.18) or (ORG, 2.01; 95% CI, 1.27–3.19). CMA showed a trend of an association. Recursive CMA indicated that more evidence is needed to conclude on the status of significance. No significant publication bias was found. Our meta-analysis suggested that the TNF-α-308G/A polymorphism contribute to the risk of OSAHS. Further studies with larger sample should be performed to confirm our findings.