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Regulation of JAK/STAT signal pathway by miR-21 in the pathogenesis of juvenile idiopathic arthritis

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World Journal of pediatrics 2020年第5期16卷 502-513页

作者： Hong-Wei Li Hua-Song Zeng department of pediatric Allergy immunology and Rheumatology Guangzhou Women and Children Medical CenterGuangzhou 510623China department of pediatric Allergy Immunology and RheumatologyGuangzhou Women and Children's Medical CenterGuangzhou Medical University9 Jinsui RoadGuangzhou 510175China

Background Overexpression of the components of the Janus kinase/signal transducer and activator of transcription(JAK/STAT)signalling pathway is the key factor of the pathogenic mechanisms underlying systemic juvenile idiopathic arthritis(sJIA).The study aims to investigate the association between miR-21 and the JAK/STAT signal pathway in JIA.Methods Total RNA was extracted from peripheral blood mononuclear cells(PBMCs)in active JIA patients.The relative expressions of miR-21,STAT3 and suppressor of cytokine signalling 3 in PBMCs were measured by real-time polymerase chain reaction and their expressions were measured by western blotting and dual-luciferase reported assay.Rheumatoid arthritis fibroblast-like synovial cell(RASF)was stimulated to become to osteoclasts using macrophage colony-stimulating factor(M-CSF)and factors that can impact on their differentiation ability were identified through the transfection of LV3-miR-21.The expression of STAT3/p-STAT3 was measured by western blot,and the levels of interleukin(IL)-17A,p65,matrix metalloproteinases(MMP)-3,MMP-4 and receptor activator of nuclear factor-κd3 after the LV3-miR-21 transfection were tested by enzyme-linked immunosorbent assay.Finally,the miR-21 targeted STAT3 gene was detected by the dualluciferase reported assay.Results The expression of miR-21 was significantly lower in JIA patients than in healthy control(P<0.05).The level of STAT3 was increased in PBMCs of JIA group compared with control group(P<0.05).Furthermore,the expression levels of miR-21 in sJIA and polyarticular JIA groups were negatively correlated with STAT3(r=-0.5854/r=-0.6134,P<0.05).The expression of STAT3 changed little in PBMCS after the stimulation of IL-6 and not in RASFs with transfection of LV3-miR-21.The expression of p-STAT3 decreased after the stimulation of IL-6 in RASFs transfected by LV3-miR-21(P<0.05).RASFs were induced into osteoclasts using M-CSF.The number of osteoclasts as determined by tartrate-resistant acid phosphatase staining was significantly lower in group m

关键词： JAK/STAT Juvenile idiopathic arthritis MiR-21 Signal transducer and activator of transcription 3 (STAT3)/p-STAT3

Effect of early atopic sensitization in children aged 0–2 years on the development of asthma symptoms at 9–11 years of age

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World Journal of pediatrics 2022年第11期18卷 753-760页

作者： Himmet Haluk Akar Ebru Nadir Burçin Beken Yakup Yeşil Division of pediatric immunology and Allergy University of Istanbul Health SciencesKanuni Sultan Suleyman Training and Research HospitalIstanbulTurkey Division of pediatrics University of Istanbul Health SciencesKanuni Sultan Suleyman Training and Research HospitalIstanbulTurkey Department of Pediatric Immunology and Allergy School of MedicineAcibadem Mehmet Ali Aydinlar UniversityIstanbulTurkey

Background Personal genetic predisposition and early life environmental factors are important for the development of childhood asthma.We aimed to search whether egg,milk and mite sensitizations at 0–2 years old are risk factors for asthma symptoms at 9–11 years old.Methods A total of 210 wheezer children who had specific immunoglobulin(Ig)E in 2010–2012 were included in the study(followed by pediatric allergy).Patients were divided into non-atopic(group 1,n=157)and atopic patients[groups 2–7,n=53(5 patients were in both group 4 and group 5)]based on sensitizations.Using the International Study of Asthma and Allergy in Childhood questionnaire,current wheeze(CW,2nd question),exercise wheezing(EW,7th question),and dry cough(DC,8th question)were surveyed.Also,parental allergies,eczema at 0–2 years,current eosinophil percentage and total IgE were recorded.Results Eczema was observed as an important risk factor[CW:odds ratio(OR)=2.83,95%confidence interval(CI)=1.54–5.23,P≤0.001;EW:OR=2.71,95%CI=1.33–5.54,P=0.006;DC:OR=3.03,95%CI=1.47–6.25,P=0.003],whereas having no atopic sensitization at 0–2-year-old(group 1)was found as a significant protective factor for asthma at 9–11 years old(CW:OR=0.32,95%CI=0.15–0.70,P=0.004;EW:OR=0.21,95%CI 0.10–0.44,P≤0.001;DC:OR=0.25,95%CI=0.10–0.59,P=0.002).Conclusion Early personal eczema is a significant risk factor for the development of asthma symptoms at 9–11 years old,whereas not having an allergic sensitization at 0–2 years old(group 1)is an important protective factor.

关键词： Asthma Children Risk factors

Genetics on early onset inflammatory bowel disease:An update

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Genes & Diseases 2020年第1期7卷 93-106页

作者： Johnson Nameirakpam Rashmi Rikhi Sanjay Singh Rawat Jyoti Sharma Deepti Suri pediatric Allergy and immunology Unit Department of PediatricsAdvanced Pediatrics CentrePostgraduate Institute of Medical Education and ResearchChandigarhIndia

Inflammatory bowel disease(IBD)is more common in adults than in children.Onset of IBD before 17 years of age is referred as pediatric onset IBD and is further categorized as very early onset IBD(VEO-IBD)for children who are diagnosed before 6 years of age,infantile IBD who had the disease before 2 years of age and neonatal onset IBD for children less than 28 days of life.Children presenting with early onset disease may have a monogenic basis.Knowledge and awareness of the clinical manifestations facilitates early evaluation and diagnosis.Next generation sequencing is helpful in making the genetic diagnosis.Treatment of childhood IBD is difficult;targeted therapies and hematopoietic stem cell transplantation form the mainstay.In this review we aim to summarize the genetic defects associated with IBD phenotype.We describe genetic location and functions of various genetic defect associated with VEO-IBD with their key clinical manifestations.We also provide clinical clues to suspect these conditions and approaches to the diagnosis of these disorders and suitable treatment options.

关键词： Il-10 signalling defect IPEX Next generation sequencing Targeted therapy Very early onset inflammatory bowel disease

An unusual cause of an anterior mediastinal mass in a 52-day-old infant with mediastinal tuberculosis

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世界儿科杂志:英文版 2016年第3期12卷 372-373页

作者： Recep Sancak Mehmet Halil Celiksoy Medical Faculty Department of Pediatric Allergy and ImmunologyOndokuz Mayıs UniversityKurupelitSamsunTurkey

Tuberculosis(TB)continues to be one of the major infectious diseases threatening millions of lives worldwide.[1]We encountered a 52-day-old male infant with a anterior mediastinal mass caused by tuberculosis.On admission to our hospital,the infant presented with respiratory distress,wheezing,fever,and cough.Decreased breath sounds were audible at the apex of the left chest.His temperature was 38.2℃.

关键词： infant tuberculosis distress

Immunological pathogenesis and treatment of systemic lupus erythematosus

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World Journal of pediatrics 2020年第1期16卷 19-30页

作者： Lu Pan Mei-Ping Lu Jing-Hua Wang Meng Xu Si-Rui Yang department of pediatric Rheumatology and Allergy The First HospitalJilin UniversityChangchunChina department of Allergy immunology and Rheumatology Children's HospitalZhejiang University School of MedicineHangzhouChina

Background Systemic lupus erythematosis(SLE)is a complex and clinically heterogeneous autoimmune disease.A variety of immunological defects contribute to SLE,including dysregulated innate and adaptive immune response.A clearer understanding of the mechanisms driving disease pathogenesis combined with recent advances in medical science is predicted to enable accelerated progress towards improved SLE-personalized approaches to treatment.The aim of this review was to clarify the immunological pathogenesis and treatment of SLE.Data sources Literature reviews and original research articles were collected from database,including PubMed and Wanfang.Relevant articles about SLE were included.Results Breakdown of self-tolerance is the main pathogenesis of SLE.The innate and adaptive immune networks are interlinked with each other through cytokines,complements,immune complexes and kinases of the intracellular machinery.Treatments targeted at possible targets of immunity have been assessed in clinical trials.Most of them did not show better safety and efficacy than traditional treatments.However,novel targeting treatments are still being explored.Conclusions Dysregulated immune response plays a critical role in SLE,including innate immunity and adaptive immunity.Biologic agents that aim to specifically target abnormal immune processes were assessing and may bring new hope to SLE patients.

关键词： Immunological pathogenesis Systemic lupus erythematosis Treatment

Autophagy modulates CD4^(+) T-cell lineage recommitment upon pathogen infection

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Cellular & Molecular immunology 2020年第7期17卷 682-683页

作者： Kai Yang Hongbo Chi department of pediatrics and the Herman B Wells Center for pediatric Research Indiana University School of MedicineIndianapolisINUSA department of Microbiology and immunology Indiana University School of MedicineIndianapolisINUSA department of immunology St.Jude Children’s Research HospitalMemphisTNUSA

The thymus provides specialized signals that support and guide the development of precursor cells into various T-cell lineages,including conventionalαβT cells comprising the CD4^(+) and CD8^(+) T-cell subsets that are key mediators of adaptive immunity.Within the thymus,a complex network of persistent T-cell receptor(TCR)activation,cytokine signals,and transcription factors dictates the development of CD4^(+) and CD8^(+) T cells.1 The fate commitment of CD4^(+) and CD8^(+) T-cell lineages is reciprocally orchestrated by the ThPOK-and Runx3-dependent transcriptome.2,3 In the periphery,mature CD4^(+) or CD8^(+) T cells are activated by specific antigens bound to major histocompatibility complex class II(MHC-II)or I(MHC-I),respectively,which facilitates their clonal expansion and effector function in defense against pathogen infection.While the dichotomy of CD4 and CD8 lineage decisions is considered to be stable in mature T cells,whether and how pathogens reprogram lineage commitment during an immune response remain unclear.In this issue of Cellular and Molecular immunology,4 Robins et al.demonstrated that Vps34/Atg7-dependent autophagy inhibits the generation of MHC-II-restricted CD4−CD8^(+) T cells by restraining Runx3 expression in effector CD4^(+) T cells upon pathogen infection(Fig.1).

关键词： Runx3 lineage infection

Infection-stimulated Anemia Results Primarily from Interferon Gamma-dependent, Signal Transducer and Activator of Transcription 1-independent Red Cell Loss

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Chinese Medical Journal 2015年第7期128卷 948-955页

作者： Zheng Wang Dong-Xia Zhang Qi Zhao department of pediatric Surgery General Hospital of Chinese People's Liberation Army Beijing 100037 China department of immunology Yuhuangding Hospital Yantai Shandong 264000 China

Background： Although the onset of anemia during infectious disease is commonly correlated with production of inflammatory cytokines, the mechanisms by which cytokines induce anemia are poorly defined. This study focused on the mechanism research. Methods： Different types of mice were infected perorally with Toxoplasma gondii strain ME49. At the indicated times, samples fi＇om each mouse were harvested, processed, and analyzed individually. Blood samples were analyzed using a Coulter Counter and red blood cell （RBC） survival was measured by biotinylation. Levels of tumor necrosis factor-α （TNF-α）, inducible nitric oxide synthase （iNOS）, and inducible protein 10 （IP-10） mRNA in liver tissue were measured by real-time polymerase chain reaction. Results： T. gondii-infected mice exhibited anemia due to a decrease in both erythropoiesis and survival time of RBC in the circulation （P 〈 0.02）. In addition, infection-stimulated anemia was associated with fecal occult, supporting previous literature that hemorrhage is a consequence of T. gondii infection in mice. Infection-induced anemia was abolished in interferon gamma （IFNy） and I FNy receptor deficient mice （P 〈 0.05） but was still evident in mice lacking TNF-α, iNOS, phagocyte NADPH oxidase or IP-10 （P 〈 0.02）. Neither signal transducer and activator of transcription 1 （STAT1） deficient mice nor 129S6 controls exhibited decreased erythropoiesis, but rather suffered from an anemia resulting solely from increased loss of circulating RBC. Conclusions： Infection-stimulated decrease in erythropoiesis and losses of RBC have distinct mechanistic bases. These results show that during T. gondii infection, IFNγ is responsible foran anemia that results from both a decrease in erythropoiesis and a STAT1 independent loss of circulating RBC.

关键词： Anemia Helnorrhage Signal Transducer and Activator of Transcription 1 Tmot）lasma gondii

The photodynamic therapy on Streptococcus mutans biofilms using erythrosine and dental halogen curing unit

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International Journal of Oral Science 2012年第4期4卷 196-201页

作者： Young-Ho Lee Ho-Won Park Ju-Hyun Lee Hyun-Woo Seo Si-Young Lee department of pediatric Dentistry Graduate SchoolCollege of DentistryGangneung-Wonju National University department of pediatric Dentistry College of DentistryGangneung-Wonju National University department of Microbiology and immunology College of DentistryGangneung-Wonju National University

The purpose of our study was to evaluate the effect of photodynamic therapy （PDT）, using erythrosine as a photosensitizing agent and a dental halogen curing unit as a light source, on Streptococcus mutans in a biofilm phase. The S. mutans biofilms were formed in a 24-well cell culture cluster. Test groups consisted of biofilms divided into four groups： group 1： no photosensitizer or light irradiation treatment （control group）; group 2： photosensitizer treatment alone; group 3： light irradiation alone; group 4： photosensitizer treatment and light irradiation. After treatments, the numbers of colony-forming unit （CFU） were counted and samples were examined by confocal laser scanning fluorescence microscopy （CLSM）. Only group 4 （combined treatment） resulted in significant increases in cell death, with rates of 75% and 55% after 8 h of incubation, and 74% and 42% at 12 h, for biofilms formed in brain-heart infusion （BHI） broth supplemented with 0% or O. 1% sucrose, respectively. Therefore, PDT of S. mutans biofilms using a combination of erythrosine and a dental halogen curing unit, both widely used in dental clinics, resulted in a significant increase in cell death. The PDT effects are decreased in biofilms that form in the presence of sucrose.

关键词： biofilms dental halogen curing unit erythrosine photodynamic therapy Streptococcus mutans

Juvenile dermatomyositis:advances in clinical presentation,myositis-specific antibodies and treatment

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World Journal of pediatrics 2020年第1期16卷 31-43页

作者： Jian-Qiang Wu Mei-Ping Lu Ann M.Reed department of Rheumatology immunology and Allergy Children's HospitalZhejiang University School of MedicineHangzhou 310052China department of pediatrics Division of Pediatric RheumatologyDuke University School of MedicineDurham 27710USA

Background Juvenile dermatomyositis(JDM)is a chronic autoimmune disease characteristic by inflammation of small vessels within the skin,muscle and vital organs.But the clinical features and treatment of JDM have not been fully clarified.Data sources Databases underwent through PubMed for articles about the clinical features,myositis-specific antibodiesof JDM and its treatment,and we selected publications written in English which were relevant to the topic of this review.Results Clinical features and myositis-specific antibodies may predict the severity and prognosis of disease.Although the mortality rate has been lower with traditional treatments,such as corticosteroid,intravenous immunoglobulin,and diseasemodifying anti-rheumatic drugs such as methotrexate,their usages are variable.Novel biological therapies seem to be effective for refractory JDM patients,but more clinical trials are necessary.Conclusions JDM is a sever disease of childhood.We need to better understand recent advances of JDM in the context of clinical features including skin manifestations,muscle weakness and organ damage,myositis-specific antibodies and their associated outcomes and the treatment of disease.

关键词： Biologic agents Extramuscular manifestations Juvenile dermatomyositis Myositis autoantibodies