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      The role of miR-29c/B7-H3 axis in children with allergic asthma

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          Abstract

          Background

          MicroRNAs play roles in the pathogenesis of bronchial asthma. However, the mechanism of miR-29c in allergic asthma remains unclear. This study is to elucidate the regulation of Th cell differentiation by miR-29c in mononuclear macrophages.

          Methods

          A total of 52 children with asthma exacerbation and 26 children as controls were enrolled in the study. CD14 + monocytes were isolated from the peripheral blood. Differential expressions of microRNAs were evaluated using microarray analysis and miR-29c expression in monocytes was determined by qRT-PCR. The plasma B7-H3 was determined by ELISA. Transfection studies and luciferase reporter assay were performed to confirm target gene of miR-29c and its function.

          Results

          Compared to controls, 88 miRNAs in blood monocytes were up-regulated and 41 miRNAs down-regulated including miR-29c in asthma children. Children with asthma exacerbation had significantly lower level of miR-29c and higher level of plasma B7-H3 compared to controls (both P < 0.05). Functional studies based on luciferase reporter assay and immunofluorescence staining suggest that B7-H3 is the direct target of miR-29c and transfection anti-miR-29c into macrophages could enhance ROR-γt and GATA-3 expression in co-cultured CD4 + T cells and increase levels of IL-4 and IL-17 in supernatants.

          Conclusion

          The axis of miR-29c/B7-H3 plays an important role in children with asthma through regulating Th2/Th17 cell differentiation and may provide new targets for treatment of asthma.

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          Most cited references25

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          MicroRNA-21 is up-regulated in allergic airway inflammation and regulates IL-12p35 expression.

          Thomas Lu, Ariel Munitz, Marc Rothenberg (2009)
          Allergic airway inflammation is characterized by marked in situ changes in gene and protein expression, yet the role of microRNAs (miRNAs), a new family of key mRNA regulatory molecules, in this process has not yet been reported. Using a highly sensitive microarray-based approach, we identified 21 miRNAs with differential expression between doxycycline-induced lung-specific IL-13 transgenic mice (with allergic airway inflammation) and control mice. In particular, we observed overexpression of miR-21 and underexpression of miR-1 in the induced IL-13 transgenic mice compared with control mice. These findings were validated in two independent models of allergen-induced allergic airway inflammation and in IL-4 lung transgenic mice. Although IL-13-induced miR-21 expression was IL-13Ralpha1 dependent, allergen-induced miR-21 expression was mediated mainly independent of IL-13Ralpha1 and STAT6. Notably, predictive algorithms identified potential direct miR-21 targets among IL-13-regulated lung transcripts, such as IL-12p35 mRNA, which was decreased in IL-13 transgenic mice. Introduction of pre-miR-21 dose dependently inhibited cellular expression of a reporter vector harboring the 3'-untranslated region of IL-12p35. Moreover, mutating miR-21 binding sites in IL-12p35 3'-untranslated region abrogated miR-21-mediated repression. In summary, we have identified a miRNA signature in allergic airway inflammation, which includes miR-21 that modulates IL-12, a molecule germane to Th cell polarization.
          Article 0 comments Cited 192 times – based on 0 reviews     Review now
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            Antagonism of microRNA-126 suppresses the effector function of TH2 cells and the development of allergic airways disease.

            Maximilian Plank, Simon Phipps, Joerg Mattes … (2009)
            Allergic asthma is an inflammatory disease of the lung characterized by abnormal T helper-2 (T(H)2) lymphocyte responses to inhaled antigens. The molecular mechanisms leading to the generation of T(H)2 responses remain unclear, although toll-like receptors (TLRs) present on innate immune cells play a pivotal role in sensing molecular patterns and in programming adaptive T cell responses. Here we show that in vivo activation of TLR4 by house dust mite antigens leads to the induction of allergic disease, a process that is associated with expression of a unique subset of small, noncoding microRNAs. Selective blockade of microRNA (miR)-126 suppressed the asthmatic phenotype, resulting in diminished T(H)2 responses, inflammation, airways hyperresponsiveness, eosinophil recruitment, and mucus hypersecretion. miR-126 blockade resulted in augmented expression of POU domain class 2 associating factor 1, which activates the transcription factor PU.1 that alters T(H)2 cell function via negative regulation of GATA3 expression. In summary, this study presents a functional connection between miRNA expression and asthma pathogenesis, and our data suggest that targeting miRNA in the airways may lead to anti-inflammatory treatments for allergic asthma.
            Article 0 comments Cited 144 times – based on 0 reviews     Review now
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              Increased frequency of dual-positive TH2/TH17 cells in bronchoalveolar lavage fluid characterizes a population of patients with severe asthma.

              Chaoyu Irvin, Iram Zafar, James A.D. Good … (2014)
              TH2 cells can further differentiate into dual-positive TH2/TH17 cells. The presence of dual-positive TH2/TH17 cells in the airways and their effect on asthma severity are unknown.
              Article 0 comments Cited 104 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Chuangli Hao: +86-512-67788302 , hcl_md@163.com
                Zhengrong Chen: +86-512-67788302 , chen_zheng_rong@163.com
                Journal
                Journal ID (nlm-ta): J Transl Med
                Journal ID (iso-abbrev): J Transl Med
                Title: Journal of Translational Medicine
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1479-5876
                Publication date (Electronic): 3 August 2018
                Publication date PMC-release: 3 August 2018
                Publication date Collection: 2018
                Volume: 16
                Electronic Location Identifier: 218
                Affiliations
                [1 ]ISNI 0000 0001 0198 0694, GRID grid.263761.7, Department of Respiratory Disease, Children’s Hospital of Soochow University, , Soochow University, ; Suzhou, China
                [2 ]ISNI 0000 0001 0198 0694, GRID grid.263761.7, Department of General Surgery, The First Affiliated Hospital of Soochow University, , Soochow University, ; Suzhou, China
                Article
                Publisher ID: 1590
                DOI: 10.1186/s12967-018-1590-8
                PMC ID: 6076420
                PubMed ID: 30075787
                SO-VID: ab7aa11b-e110-4357-91e0-46d6ca1667ff
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 29 May 2018
                Date accepted : 25 July 2018
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81771676
                Award ID: 81570016
                Award Recipient :
                Funded by: Social Development Projects of Jiangsu Province
                Award ID: BE2016676
                Award Recipient :
                Funded by: Jiangsu Provincial Medical Youth Talent
                Award ID: QNRC2016766
                Award Recipient :
                Funded by: Key Lab of Respiratory Disease of Suzhou
                Award ID: SZS201714
                Award Recipient :
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Medicine
                Keywords: asthma,children,mircorna,b7-h3,th cell differentiation
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: asthma, children, mircorna, b7-h3, th cell differentiation

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