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dc.contributor.authorHonkanen, Jarno
dc.contributor.authorVuorela, Arja
dc.contributor.authorMuthas, Daniel
dc.contributor.authorOrivuori, Laura
dc.contributor.authorLuopajärvi, Kristiina
dc.contributor.authorTejesvi, Mysore Vishakante Gowda
dc.contributor.authorLavrinienko, Anton
dc.contributor.authorPirttilä, Anna Maria
dc.contributor.authorFogarty, Christopher L.
dc.contributor.authorHärkönen, Taina
dc.contributor.authorIlonen, Jorma
dc.contributor.authorRuohtula, Terhi
dc.contributor.authorKnip, Mikael
dc.contributor.authorKoskimäki, Janne J.
dc.contributor.authorVaarala, Outi
dc.date.accessioned2020-04-21T14:43:15Z
dc.date.available2020-04-21T14:43:15Z
dc.date.issued2020
dc.identifier.citationHonkanen, J., Vuorela, A., Muthas, D., Orivuori, L., Luopajärvi, K., Tejesvi, M. V. G., Lavrinienko, A., Pirttilä, A. M., Fogarty, C. L., Härkönen, T., Ilonen, J., Ruohtula, T., Knip, M., Koskimäki, J. J., & Vaarala, O. (2020). Fungal Dysbiosis and Intestinal Inflammation in Children With Beta-Cell Autoimmunity. <i>Frontiers in Immunology</i>, . <a href="https://doi.org/10.3389/fimmu.2020.00468" target="_blank">https://doi.org/10.3389/fimmu.2020.00468</a>
dc.identifier.otherCONVID_35251059
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/68636
dc.description.abstractAlthough gut bacterial dysbiosis is recognized as a regulator of beta-cell autoimmunity, no data is available on fungal dysbiosis in the children at the risk of type 1 diabetes (T1D). We hypothesized that the co-occurrence of fungal and bacterial dysbiosis contributes to the intestinal inflammation and autoimmune destruction of insulin-producing beta-cells in T1D. Fecal and blood samples were collected from 26 children tested positive for at least one diabetes-associated autoantibody (IAA, GADA, IA-2A or ICA) and matched autoantibody-negative children with HLA-conferred susceptibility to T1D (matched for HLA-DQB1 haplotype, age, gender and early childhood nutrition). Bacterial 16S and fungal ITS2 sequencing, and analyses of the markers of intestinal inflammation, namely fecal human beta-defensin-2 (HBD2), calprotectin and secretory total IgA, were performed. Anti-Saccharomyces cerevisiae antibodies (ASCA) and circulating cytokines, IFNG, IL-17 and IL-22, were studied. After these analyses, the children were followed for development of clinical T1D (median 8 years and 8 months). Nine autoantibody positive children were diagnosed with T1D, whereas none of the autoantibody negative children developed T1D during the follow-up. Fungal dysbiosis, characterized by high abundance of fecal Saccharomyces and Candida, was found in the progressors, i.e., children with beta-cell autoimmunity who during the follow-up progressed to clinical T1D. These children showed also bacterial dysbiosis, i.e., increased Bacteroidales and Clostridiales ratio, which was, however, found also in the non-progressors, and is thus a common nominator in the children with beta-cell autoimmunity. Furthermore, the progressors showed markers of intestinal inflammation detected as increased levels of fecal HBD2 and ASCA IgG to fungal antigens. We conclude that the fungal and bacterial dysbiosis, and intestinal inflammation are associated with the development of T1D in children with beta-cell autoimmunity.en
dc.format.mimetypeapplication/pdf
dc.languageeng
dc.language.isoeng
dc.publisherFrontiers Media
dc.relation.ispartofseriesFrontiers in Immunology
dc.rightsCC BY 4.0
dc.subject.othermycobiome
dc.subject.otherdysbiosis
dc.subject.othergut
dc.subject.otherinflammation
dc.subject.otherCandida
dc.subject.otherSaccharomyces
dc.subject.othertype 1 diabetes
dc.titleFungal Dysbiosis and Intestinal Inflammation in Children With Beta-Cell Autoimmunity
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-202004212845
dc.contributor.laitosBio- ja ympäristötieteiden laitosfi
dc.contributor.laitosDepartment of Biological and Environmental Scienceen
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.type.coarhttp://purl.org/coar/resource_type/c_2df8fbb1
dc.description.reviewstatuspeerReviewed
dc.relation.issn1664-3224
dc.type.versionpublishedVersion
dc.rights.copyright© 2020 the Authors
dc.rights.accesslevelopenAccessfi
dc.subject.ysoautoimmuunisairaudet
dc.subject.ysoautoimmuniteetti
dc.subject.ysonuoruustyypin diabetes
dc.subject.ysosuolistomikrobisto
dc.subject.ysohiivasienet
dc.subject.ysotulehdus
dc.format.contentfulltext
jyx.subject.urihttp://www.yso.fi/onto/yso/p16178
jyx.subject.urihttp://www.yso.fi/onto/yso/p21598
jyx.subject.urihttp://www.yso.fi/onto/yso/p19788
jyx.subject.urihttp://www.yso.fi/onto/yso/p37925
jyx.subject.urihttp://www.yso.fi/onto/yso/p6486
jyx.subject.urihttp://www.yso.fi/onto/yso/p1049
dc.rights.urlhttps://creativecommons.org/licenses/by/4.0/
dc.relation.doi10.3389/fimmu.2020.00468
jyx.fundinginformationThis work was supported by the Finnish Cultural Foundation (JH), the Finnish Diabetes Research Foundation (JH and OV), the Academy of Finland (OV), the Päivikki and Sakari Sohlberg Foundation (OV), and European Foundation for the Study of Diabetes (OV).
dc.type.okmA1


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