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Alopecia areata (AA) is an immune‐mediated chronic alopecia disease, but its specific pathogenesis is unclear. Gene expression data for AA patients (AAs) and healthy controls (HCs) were retrieved from the GEO database, and the differentially expressed genes (DEGs) between AAs and HCs were identified. Then, GO, KEGG and GSEA analysis were performed. A PPI network for the DEGs was then constructed to screen for hub genes, which were validated by three additional datasets. Subsequently, the potential miRNAs interacting with the hub genes were obtained through TarBase and miRNet. The differentially expressed lncRNAs (DElncRs) were obtained for subcellular localisation analysis, and the DElncRs located in the cytoplasm were further screened to identify miRNAs that interact with them. The shared miRNAs interacting with the hub genes and lncRNAs were used to construct a network of mRNA‐miRNA‐lncRNA interactions. Lastly, ROC analysis was performed to evaluate the potential diagnostic value of the hub genes and DElncRs identified. A total of 173 DEGs were obtained, mainly enriched in cytokines, chemokines, hair follicle development and hair cycle related signalling pathways. Through PPI screening and validation based on 3 additional datasets, 24 hub genes were finally yielded. Of them, five hub genes were upregulated and the potential miRNAs that interact with these five hub genes were identified. Additionally, 26 DElncRs were obtained, including 9 upregulated lncRNAs located in the cytoplasm that were predicted to interact with the miRNAs. Finally, an mRNA‐miRNA‐lncRNA regulatory network was constructed using five hub genes, four lncRNAs and their shared five miRNAs. The regulatory relationship between CD8A, mir‐185‐5p and FOXD2‐AS1 might be crucial in AA pathogenesis, with CD8A and FOXD2‐AS1 exhibiting diagnostic potential. CD8A and FOXD2‐AS1 may serve as potential therapeutic targets in AA. [ABSTRACT FROM AUTHOR]

Chronic spontaneous urticaria (CSU) is a mast cell‐driven disease with many advances in its aetiology and pathogenesis over the past years. The main treatment of CSU is oral second‐generation antihistamines. However, only an average of 50% of CSU patients responded adequately to conventional or quadruple doses of non‐sedative antihistamines. Meanwhile, gut microbiota can affect the efficacy of drugs. The purpose of this study was to investigate the relationship between gut microbiota and the efficacy of antihistamines in patients with CSU. The patients with CSU were divided into responders and non‐responders according to the efficacy of antihistamine monotherapy. The gut microbiota of faecal samples from 15 responders and 15 non‐responders was detected by 16S rDNA sequencing, and the differential bacterial species between the two groups were verified by quantitative polymerase chain reaction (qPCR). Additional faecal samples from 30 responders and 30 non‐responders were used as an extended cohort to further verify the above differential bacterial species by qPCR. Lachnospiraceae and its subordinate taxa were found to be the main differences in gut microbiota between responders and non‐responders. The abundance of Lachnospira in responders was higher than that in non‐responders. Lachnospira exhibits moderate diagnostic value in evaluating the efficacy of antihistamine. Lachnospira is a signature for predicting the efficacy of antihistamine in patients with CSU. [ABSTRACT FROM AUTHOR]

These results indicated that ADO may be a new candidate biomarker for predicting disease activity and the treatment outcome of patients with CSU. In conclusion, we investigated plasma ADO level in CSU patients, and its potential use as a biomarker for predicting disease activity and response to the conventional dose of H1-antihistamine treatment. [Extracted from the article]