BackgroundInterleukin-35 (IL-35) is a recently discovered cytokine that plays a role in immune suppression and has therefore been the subject of a great deal of research. A bibliometric analysis of the global research concerning IL-35, however, is rare.ObjectivesThe aim of this research was to assess the international scientific output of IL-35 research and explore its hotspots and frontiers from 2009 to 2018 by bibliometric analysis.MethodsPublications about IL-35 research from 2009 to 2018 were retrieved from the Web of Science Core Collection (WoSCC). Citespace V was used to analyze years, journals, countries, research institutions, areas of exploration, research hotspots, and trends of publication.ResultsWe retrieved a total of 416 publications and observed a trend of publications increasing over the past decade. Original articles (351) were the most frequently occurring document type. The largest number of publications belonging to one country and one institution, respectively, was China (202) and Tianjin Medical University (17). Trending keywords may indicate frontier topics, including “infectious tolerance,” “autoimmune,” and “central nervous system.”ConclusionThis study provides valuable information on the study of IL-35 so that researchers may identify new research fields.
Background Genetic background is one of the important risk factors for development of asthma. The nucleotide‐binding oligomerization domain 2 (NOD2) has been involved in the pathogenesis of asthma. The purpose of this study was to explore the relationship between NOD2 gene polymorphisms and asthma susceptibility in the Chinese Han population. Methods Children with asthma (n = 309) and Healthy children (n = 163) were recruited from Yancheng Third People's Hospital, Yancheng, China, between January 2016 and December 2017. The NOD2 gene polymorphisms were measured by the Snapshot SNP genotyping assays. Genotyping was performed for 4 tag SNPs of NOD2. Serum IFN‐β levels were measured by ELISA. Results The serum IFN‐β levels were significantly lower in Asthmatic children than those in the controls (p < 0.001). Low levels of IFN‐β may be related to the susceptibility to severe asthma. The rs3135499 C allele was associated with a significantly increased risk of asthma as compared with the rs3135499 A allele. Conclusion The rs3135499 polymorphism of NOD2 gene and IFN‐β may play a role in the pathogenesis of asthma.
Background Lower respiratory tract infection (LRTI) is one of the leading cause of death in children under 5 years old around the world between 1980 and 2016. Distinguishing between viral and bacterial infection is challenging when children suffered from LRTI in the absence of pathogen detection. The aim of our study is to analyze the difference of serum β2-microglobulin (β2-MG) between viral LRTI and bacterial LRTI in children. Methods This retrospective study included children with LRTI caused by a single pathogen from Yancheng Third People’s Hospital, Yancheng, China, between January 1, 2016 and December 31, 2019. Participants were divided into the younger group (1 year old ≤ age < 3 years old) and the older group (3 years old ≤ age < 5 years old) for subgroup analysis. Results A total of 475 children with LRTI caused by common respiratory pathogens were identified. In the younger group as well as the older group, the serum level of β2-MG in respiratory syncytial virus, influenza A virus and influenza B virus groups were significantly increased compared to that in the Mycoplasma pneumoniae group. Compared with Streptococcus pneumoniae infection group, the serum β2-MG level of respiratory syncytial virus, influenza A virus and influenza B virus groups were significantly higher in children between 1 and 3 years old. Conclusions The serum β2-MG may distinguish viral infection from bacterial infection in children with LRTI.
Obesity and dyslipidemia are two metabolic syndrome disorders that have serious effects on the health of patients. Purinergic 2X receptor ligand-gated ion channel 7 (P2X7R) has been reported to play a role in regulating lipid storage and metabolism. However, the role and potential mechanism of P2X7R in adipogenesis and lipid degradation remain unknown. In the present study, a mouse model of obesity was established by feeding mice a high-fat diet, and the 3T3-L1 cell line was used to analyze the function of P2X7R in vitro. Reverse transcription-quantitative PCR and western blot analyses were performed to detect the expression levels of P2X7R, sterol regulatory element-binding protein 1 (SREBP1) and other associated transcription factors. Bioinformatics analysis was used to predict the potential target gene of P2X7R and a dual luciferase reporter assay was used to confirm this prediction. Oil Red O staining was used to evaluate the adipogenic capacity of preadipocytes. AdipoRed assay, cholesterol assay and a free glycerol reagent were used to measure the expression levels of triglyceride (TGs), total cholesterol (TC) and glycerin, respectively. The results indicated that P2X7R was highly expressed in obese mice and that it was involved in adipogenic differentiation in vitro. SREBP1 enhanced the transcription activities of P2X7R to promote its expression. Inhibition of P2X7R significantly reduced the adipogenic capacity of preadipocytes, decreased the expression levels of adipogenesis-associated transcription factors (peroxisome proliferator-activated receptor γ, CCAAT-enhancer-binding protein α and fatty-acid-binding protein 4), enhanced the expression levels of lipolytic enzymes (adipose triglyceride lipase, phosphorylated hormone-sensitive lipase and monoacylglycerol lipase) and regulated the expression of TG, TC and glycerin in mature 3T3-L1 cells. These effects were reversed by a small interfering RNA targeting Wnt3a. Therefore, the results suggested that P2X7R, the transcription activities of which were regulated by SREBP1, regulated adipogenesis and lipid degradation by targeting SREBP1, indicating its potential effects on obesity-associated metabolism.
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