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Article ; Online: Editorial

Lingli Dong / Hisanori Umehara / Jixin Zhong

Frontiers in Medicine, Vol

Rheumatic Diseases and Infection

2022 Volume 9

Keywords	infection ; rheumatic disease ; virus ; autoimmune disease (AID) ; inflammatory ; Medicine (General) ; R5-920
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Epidemiology and Clinical Management of Rheumatic Autoimmune Diseases in the COVID-19 Pandemic

Yingzi Zhu / Jixin Zhong / Lingli Dong

Frontiers in Medicine, Vol

A Review

2021 Volume 8

Abstract: The coronavirus disease 2019 (COVID-19) has been in pandemic for more than 1 year, with serious negative effects produced worldwide. During this period, there have been a lot of studies on rheumatic autoimmune diseases (RADs) combined with COVID-19. The ... ...

Abstract	The coronavirus disease 2019 (COVID-19) has been in pandemic for more than 1 year, with serious negative effects produced worldwide. During this period, there have been a lot of studies on rheumatic autoimmune diseases (RADs) combined with COVID-19. The purpose of this study is to review and summarize these experiences. Pubmed, Web of science, Embase and the Cochrane library were searched from January 15, 2020 to July 15, 2021 using RADs and COVID-19 related keywords. Based on a comprehensive review of studies covering 16 countries, the prevalence of COVID-19 does not necessarily increase in RADs patients compared to the general population. In RADs population infected with COVID-19, a high proportion of female patients (54.44~95.2%), elderly patients (≥50y, 48~75.88%), and patients with pre-existing comorbidities (respiratory, 4.8~60.4%; endocrine, 8.52~44.72%; cardiovascular, 15.7~64.73%) were observed, although, this does not appear to have a decisive effect on disease severity. Many anti-rheumatic treatments have been extensively evaluated for their efficacy of treating COVID-19 in RADs patients, with TNF-α inhibitors and IL-6 receptor antagonist receiving more positive reviews. However, there is no conclusive information for most of the therapeutic regimens due to the lack of high-level evidence. Inflammatory markers or neutrophil-lymphocyte-ratio may be applied as indicators for clinical prognosis or therapeutic regimens adjustment. Thus, more research is still needed to address the prevalence, treatment, and clinical monitoring of RADs patients in COVID-19 pandemic.
Keywords	rheumatic autoimmune diseases ; COVID-19 ; prevalence ; treatment ; laboratory indicator ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2021-08-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: IL-33 in Rheumatic Diseases

Yuanji Dong / Jixin Zhong / Lingli Dong

Frontiers in Medicine, Vol

2021 Volume 8

Abstract: Interleukin-33 (IL-33) is a nuclear factor mainly expressed in barrier epithelium, endothelial cells, and fibroblast reticular cells. Some inflammatory cells also express IL-33 under certain conditions. The important role of IL-33 in allergic reactions, ... ...

Abstract	Interleukin-33 (IL-33) is a nuclear factor mainly expressed in barrier epithelium, endothelial cells, and fibroblast reticular cells. Some inflammatory cells also express IL-33 under certain conditions. The important role of IL-33 in allergic reactions, helminth infection, cancer, tissue fibrosis, chronic inflammation, organ transplantation, and rheumatic immune diseases has been extensively studied in recent years. IL-33 primarily activates various circulating and tissue-resident immune cells, including mast cell, group 2 innate lymphoid cell (ILC2), regulatory T cell (Treg), T helper 2 cell (Th2), natural killer cell (NK cell), and macrophage. Therefore, IL-33 plays an immunomodulatory role and shows pleiotropic activity in different immune microenvironments. The IL-33/serum stimulation-2 (ST2) axis has been shown to have a detrimental effect on rheumatoid arthritis, systemic lupus erythematosus, and other rheumatic diseases. Interestingly, IL-33 also plays a protective role in the repair of barrier epithelium and the activation of Tregs. Therefore, the role of IL-33/ST2 depends on the underlying pathological conditions in rheumatic diseases. This review focuses on the dual role of the IL-33/ST2 axis in rheumatic diseases.
Keywords	IL-33 ; alarmin ; ST2 ; autoimmune ; rheumatic disease ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Structural Lesion Progression of the Sacroiliac Joint and Clinical Features in axSpA During TNFi Reduction

Qian Mo / Yuanji Dong / Cong Ye / Jixin Zhong / Shaozhe Cai / Min Wang / Lingli Dong

Frontiers in Medicine, Vol

A Retrospective Cohort Study

2021 Volume 8

Abstract: Objective: In the clinic, some patients with axial spondyloarthritis (axSpA) have to reduce tumor necrosis factor inhibitor (TNFi) for various reasons. However, there are few studies about how to balance the relapse and TNFi reduction. Here we ... ...

Abstract	Objective: In the clinic, some patients with axial spondyloarthritis (axSpA) have to reduce tumor necrosis factor inhibitor (TNFi) for various reasons. However, there are few studies about how to balance the relapse and TNFi reduction. Here we retrospectively analyzed the structural progression of the sacroiliac joint (SIJ) and clinical features in axSpA during TNFi reduction.Methods: A total of 108 patients with axSpA who followed up for 2 years and completed at least baseline, 12-month, and 24-month MRI scans of SIJ were divided into the tapering group (n = 63) and withdrawal group (n = 45) according to whether TNFi was stopped. We divided 2 years into five intervals, calculating the average dose quotient (DQ) for each of 540 intervals from 108 patients. By using generalized estimation equations with inverse probability of treatment weighting, we investigated the unbiased effects of average DQ on structural progression and treatment response.Results: The disease activity (such as Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI), Ankylosing Spondylitis Disease Activity Score (ASDAS)-CRP, and ASDAS-ESR) and relapse rate were lower in the tapering group at 12 and 24 months (p < 0.05). Δerosion (β = −0.0100, p = 0.00026) and Δthe Spondyloarthritis Research Consortium of Canada (SPARCC; β = −0.0959, p < 0.0001) were negatively correlated with average DQ. The average DQ 30 (74.8%, 80.0%) or 41.6 (76.5%, 83%) was best to discriminate the status of treatment response or the status of bone marrow edema, but considering operability, the average DQ 25 (78.0%, 63.3%) was also acceptable especially for patients with HLA-B27 negative and non-severe fat metaplasia.Conclusion: Complete TNFi withdrawal was not recommended. Our study provided a referable strategy (tapering then maintained the average DQ over 30 or even 25) for patients who need TNFi reduction. Higher dose usage of TNFi was associated with a slower erosion progression of SIJ.
Keywords	axial spondyloarthritis ; tumor necrosis factor inhibitor ; tapering ; sacroiliac joint ; magnetic resonance imaging ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2021-12-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Linggui Zhugan Decoction activates the SIRT1-AMPK-PGC1α signaling pathway to improve mitochondrial and oxidative damage in rats with chronic heart failure caused by myocardial infarction

Siyi Yu / Hang Qian / Dawei Tian / Mingming Yang / Dongfeng Li / Hao Xu / Jishun Chen / Jingning Yang / Xincai Hao / Zhixin Liu / Jixin Zhong / Handong Yang / Xinlong Chen / Xinwen Min / Jun Chen

Frontiers in Pharmacology, Vol

2023 Volume 14

Abstract: Objective: To investigate the effects of Linggui Zhugan Decoction on mitochondrial and oxidative damage in rats with chronic heart failure after myocardial infarction and the related mechanisms.Methods: Chronic heart failure after myocardial infarction ... ...

Abstract	Objective: To investigate the effects of Linggui Zhugan Decoction on mitochondrial and oxidative damage in rats with chronic heart failure after myocardial infarction and the related mechanisms.Methods: Chronic heart failure after myocardial infarction was established by coronary artery ligation. Heart failure rats were randomly divided into three groups: Model group (n = 11), Linggui Zhugan Decoction group (n = 12), and captopril group (n = 11). Rats whose coronary arteries were only threaded and not ligated were sham group (n = 11). Cardiac function, superoxide dismutase (SOD), malondialdehyde (MDA) contents, soluble growth-stimulating expression factor (ST2), and N-terminal B-type brain natriuretic peptide precursor (NTproBNP) levels were analyzed after treatment. Moreover, the level of mitochondrial membrane potential was detected by JC-1 staining, the ultrastructural of myocardial mitochondria were observed by transmission electron microscopy. The related signal pathway of silent information regulator factor 2-related enzyme 1 (SIRT1), adenylate activated protein kinase (AMPK), phosphorylated adenylate activated protein kinase (p-AMPK), and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is an important pathway to regulate mitochondrial energy metabolism, and to initiate mitochondrial biogenesis. The expression level was detected by Western blot and reverse transcription to explore the mechanism of the decoction.Results: Compared with the model rats, Linggui Zhugan Decoction significantly improved cardiac function (p < 0.05), reduced MDA production (p < 0.01), increased SOD activity (p < 0.05), reduced ST-2(p < 0.01), and NT-proBNP(p < 0.05) levels, increased mitochondrial membrane potential, and improved mitochondria function. In addition, Linggui Zhugan Decoction upregulated the expression of SIRT1, p-AMPK, PGC-1α protein, and mRNA in cardiac myocytes.Conclusion: Linggui Zhugan Decoction can improve the cardiac function of heart failure rats by enhancing myocardial ...
Keywords	mitochondria ; heart failure ; myocardial infarction ; animal experiments ; traditional Chinese medicine ; Therapeutics. Pharmacology ; RM1-950
Subject code	610
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Intratracheal Poly(I:C) Exposure Accelerates the Immunological Disorder of Salivary Glands in Sjogren's-Like NOD/ShiLtJ Mice

Peng Hu / Bingxia Ming / Xuefen Wu / Shaozhe Cai / Jungen Tang / Yuanji Dong / Tianshu Zhou / Zheng Tan / Jixin Zhong / Fang Zheng / Lingli Dong

Frontiers in Medicine, Vol

2021 Volume 8

Abstract: Evidences have suggested that Sjogren's syndrome (SS) is associated with viral infection. The aim of this study was to investigate the involvement of respiratory viral poly(I:C) in the pathogenesis of SS and potential mechanisms using a SS-like NOD/ ... ...

Abstract	Evidences have suggested that Sjogren's syndrome (SS) is associated with viral infection. The aim of this study was to investigate the involvement of respiratory viral poly(I:C) in the pathogenesis of SS and potential mechanisms using a SS-like NOD/ShiLtJ (NOD) mouse model. 5-week female NOD mice were intratracheally administered poly(I:C) every other day for 5 times to mimic viral infection. Pilocarpine induced saliva secretion was determined every 8 days. Submandibular glands (SMG) and lungs were harvested for the detection of pathological changes. We found that intratracheal administration of poly(I:C) significantly advanced and enhanced the reduction of saliva flow rate in NOD mice. Furthermore, poly(I:C) treatment aggravated the histopathological lesions and inflammatory cells infiltration in SMG. Accompanied by elevated expression of IFN cytokines and IL-33, Th1 activation was enhanced in SMG of poly(I:C)-treated NOD mice, but Th17 cells activation was unchanged among the groups. In addition, intratracheal poly(I:C) exposure promoted the expression of IL-33 and increased T cells proportion in the lung, which were consistent with the change in SMG. Therefore, intratracheal poly(I:C) exposure aggravated the immunological and function disorder of SMG in NOD mice.
Keywords	Sjogren's syndrome ; poly(I:C) ; salivary gland ; immune response ; IL-33 ; Medicine (General) ; R5-920
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Comprehensive expression analysis of miRNA in breast cancer at the miRNA and isomiR levels

Wu, Xianjin / Jixin Zhong / Junfa Xu / Lawei Yang / Rong Zeng / Shaoke Wu

Gene. 2015 Feb. 25, v. 557

2015

Abstract: Breast cancer (BC) is the main factor that leads cause of cancer death in women worldwide. A class of small non-coding RNAs, microRNAs (miRNAs), has been widely studied in human cancers as crucial regulatory molecule. Recent studies indicate that a ... ...

Abstract	Breast cancer (BC) is the main factor that leads cause of cancer death in women worldwide. A class of small non-coding RNAs, microRNAs (miRNAs), has been widely studied in human cancers as crucial regulatory molecule. Recent studies indicate that a series of isomiRs can be yielded from a miRNA locus, and these physiological miRNA isoforms have versatile roles in miRNA biogenesis. Herein, we performed a comprehensive analysis of miRNAs at the miRNA and isomiR levels in BC using next-generation sequencing data from The Cancer Genome Atlas (TCGA). Abnormally expressed miRNA (miR-21, miR-221, miR-155, miR-30e and miR-25) and isomiR profiles could be obtained at the miRNA and isomiR levels, and similar biological roles could be detected. IsomiR expression profiles should be further concerned, and especially isomiRs are actual regulatory molecules in the miRNAâmRNA regulatory networks. The study provides a comprehensive expression analysis at the miRNA and isomiR levels in BC, which indicates biological roles of isomiRs.
Keywords	biogenesis ; breast neoplasms ; death ; genome ; high-throughput nucleotide sequencing ; humans ; loci ; microRNA ; non-coding RNA ; women
Language	English
Dates of publication	2015-0225
Size	p. 195-200.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2014.12.030
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Sphingomyelin synthase 1 enhances BCR signaling to promote lupus-like autoimmune responseResearch in Context

Chenqiong Wang / Bingxia Ming / Xuefen Wu / Tong Wu / Shaozhe Cai / Peng Hu / Jungen Tang / Zheng Tan / Chaohong Liu / Jixin Zhong / Fang Zheng / Lingli Dong

EBioMedicine, Vol 45, Iss , Pp 578-

2019 Volume 587

Abstract: Background: Sphingomyelin synthase 1 (SMS1) has been reported to participate in hepatitis and atherosclerosis. However, its role in autoimmune response is not clear. This study investigates the possible involvement of SMS1 in B-cell activation and lupus- ... ...

Abstract	Background: Sphingomyelin synthase 1 (SMS1) has been reported to participate in hepatitis and atherosclerosis. However, its role in autoimmune response is not clear. This study investigates the possible involvement of SMS1 in B-cell activation and lupus-like autoimmunity. Methods: SMS1 knockout lupus-like animal model and SLE patient samples were utilized. B-cell activation and associated signal transduction were detected by flow cytometry, confocal analysis and western blotting. The SMS1 expression in B cells was measured by real-time qPCR. Findings: SMS1 deficiency suppressed B-cell activation in culture, which was restored by exogenous SM supplementation. The BCR-mediated early signal transduction including the colocalization of BCR with F-actin or pY/pBtk, and the phosphorylation of intracellular Fyn and Syk were impaired in SMS1 knockout B cells. Furthermore, SMS1 knockout mice showed reduced production and deposition of autoantibodies, accompanied by less severe kidney pathological changes after pristane induction. SMS1 deficiency also displayed lower autoantibody titers and 24 h urine protein excretion in bm12-induced lupus, which were associated with reduced B-cell activation. Adoptively transferred wide-type B cells partially recovered B-cell activation and autoantibody production in SMS1 deficient bm12-induced lupus mice. Moreover, the SMS1 mRNA level in B cells of SLE patients was increased and positively correlated with the serum anti-dsDNA level, IgG and globulin titers. Interpretation: These data suggest that SMS1 is involved in lupus-like autoimmunity via regulating BCR signal transduction and B cell activation. (Word count for the abstract: 230). Keywords: Systemic lupus erythematosus, Sphingomyelin synthase 1, B cell, B cell receptor
Keywords	Medicine ; R ; Medicine (General) ; R5-920
Subject code	571 ; 616
Language	English
Publishing date	2019-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Oxidized LDL upregulates macrophage DPP4 expression via TLR4/TRIF/CD36 pathwaysResearch in context

Xiaoquan Rao / Shi Zhao / Zachary Braunstein / Hong Mao / Michael Razavi / Lihua Duan / Yingying Wei / Amelia C. Toomey / Sanjay Rajagopalan / Jixin Zhong

EBioMedicine, Vol 41, Iss , Pp 50-

2019 Volume 61

Abstract: Background: We and others have shown that dipeptidyl peptidase-IV (DPP4) expression is increased in obesity/atherosclerosis and is positively correlated with atherosclerotic burden. However, the mechanism by which DPP4 expression is regulated in obesity ... ...

Abstract	Background: We and others have shown that dipeptidyl peptidase-IV (DPP4) expression is increased in obesity/atherosclerosis and is positively correlated with atherosclerotic burden. However, the mechanism by which DPP4 expression is regulated in obesity remains unclear. In this study, we investigated the pathways regulating the expression of DPP4 on macrophages. Methods: Flowsight® Imaging Flow Cytometry was employed for the detection of DPP4 and immunophenotyping. DPP4 enzymatic activity was measured by a DPPIV-Glo™ Protease Assay kit. Findings: Human monocytes expressed a moderate level of membrane-bound DPP4. Obese patients with body mass index (BMI) ≥ 30 had a higher level of monocyte DPP4 expression, in parallel with higher levels of HOMA-IR, blood glucose, triglycerides, and non-HDL cholesterol, compared to those in the non-obese (BMI < 30) patients. Oxidized low-density lipoprotein (oxLDL), but not native LDL, up-regulated DPP4 expression on macrophages with a preferential increase in CD36+ cells. OxLDL mediated DPP4 up-regulation was considerably diminished by Toll-like receptor-4 (TLR4) knockdown and CD36 deficiency. TRIF deficiency, but not MyD88 deficiency, attenuated oxLDL-induced DPP4 increase. Interpretation: Our study suggests a key role for oxLDL and downstream CD36/TLR4/TRIF in regulating DPP4 expression. Increased DPP4 in response to oxidized lipids may represent an integrated mechanism linking post-prandial glucose metabolism to lipoprotein abnormality-potentiated atherosclerosis. Keywords: Dipeptidyl peptidase IV, Inflammation, Obesity, Atherosclerosis, Oxidized LDL
Keywords	Medicine ; R ; Medicine (General) ; R5-920
Subject code	616
Language	English
Publishing date	2019-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Differential contribution of bone marrow-derived infiltrating monocytes and resident macrophages to persistent lung inflammation in chronic air pollution exposure

Roopesh Singh Gangwar / Vinesh Vinayachandran / Palanivel Rengasamy / Ricky Chan / Bongsoo Park / Rachel Diamond-Zaluski / Elaine Ann Cara / Anthony Cha / Lopa Das / Courteney Asase / Andrei Maiseyeu / Jeffrey Deiuliis / Jixin Zhong / Wayne Mitzner / Shyam Biswal / Sanjay Rajagopalan

Scientific Reports, Vol 10, Iss 1, Pp 1-

2020 Volume 15

Abstract: Abstract Chronic exposure to particulate matter < 2.5µ (PM2.5) has been linked to cardiopulmonary disease. Tissue-resident (TR) alveolar macrophages (AΦ) are long-lived, self-renew and critical to the health impact of inhalational insults. There is an ... ...

Abstract	Abstract Chronic exposure to particulate matter < 2.5µ (PM2.5) has been linked to cardiopulmonary disease. Tissue-resident (TR) alveolar macrophages (AΦ) are long-lived, self-renew and critical to the health impact of inhalational insults. There is an inadequate understanding of the impact of PM2.5 exposure on the nature/time course of transcriptional responses, self-renewal of AΦ, and the contribution from bone marrow (BM) to this population. Accordingly, we exposed chimeric (CD45.2/CD45.1) mice to concentrated PM2.5 or filtered air (FA) to evaluate the impact on these end-points. PM2.5 exposure for 4-weeks induced an influx of BM-derived monocytes into the lungs with no contribution to the overall TR-AΦ pool. Chronic (32-weeks) PM2.5 exposure on the other hand while associated with increased recruitment of BM-derived monocytes and their incorporation into the AΦ population, resulted in enhanced apoptosis and decreased proliferation of TR-AΦ. RNA-seq analysis of isolated TR-AΦ and BM-AΦ from 4- and 32-weeks exposed mice revealed a unique time-dependent pattern of differentially expressed genes. PM2.5 exposure resulted in altered histological changes in the lungs, a reduced alveolar fraction which corresponded to protracted lung inflammation. Our findings suggest a time-dependent entrainment of BM-derived monocytes into the AΦ population of PM2.5 exposed mice, that together with enhanced apoptosis of TR-AΦ and reorganization of transcriptional responses, could collectively contribute to the perpetuation of chronic inflammation.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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