<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY alias="ena-STUDY-UNIVERSITY OF COPENHAGEN-05-01-2016-13:23:48:762-578" center_name="University of Copenhagen" accession="ERP013759">
    <IDENTIFIERS>
      <PRIMARY_ID>ERP013759</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject">PRJEB12298</EXTERNAL_ID>
      <SUBMITTER_ID namespace="UNIVERSITY OF COPENHAGEN">ena-STUDY-UNIVERSITY OF COPENHAGEN-05-01-2016-13:23:48:762-578</SUBMITTER_ID>
      <SUBMITTER_ID namespace="University of Copenhagen">ena-STUDY-UNIVERSITY OF COPENHAGEN-05-01-2016-13:23:48:762-578</SUBMITTER_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Gut microbiota characterization of CD1d-dependent NKT cells knockout mice before and after induction of contact hypersensitivity</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>CD1d-dependent natural killer T (CD1d-NKT) cells play a prominent role in down-regulating aggravated reactions of contact hypersensitivity (CHS), partly through stimulation of IL-10 producing Bregs and possibly mediated via alterations of gut microbiota (GM) composition. We characterized the GM composition (high-throughput 16S rRNA gene-amplicon sequencing) of CD1d knockout (CD1d-KO) and wild-type (Wt) mice before and after contact with contact-allergen-exposure (dinitrochlorobenzene [DNCB]). Prior to CHS induction, we demonstrate that absence of CD1d-NKT cells simultaneously promote (e.g. YS2 bacteria) and limit (e.g. Butyricimonas and an unclassified genus of the Enterobacteriaceae) the presence of rare bacterial members. Further, CD1d-KO tended to harbor a more diverse GM compared to Wt. Upon induction,  the relative abundance of genera belonging to Clostridiales and Bacteroidales  increased in CD1d KO mice, as compared to their Wt littermates. These observations could implicate that changes in GM distribution driven by CD1d-NKT towards a hypersensitivity-tolerance composition may conform a regulatory mechanism for stimulation of IL-10 producing Bregs, which could further help to counteract aggravated reactions of CHS.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>Gut microbiota characterization of CD1d-dependent NKT cells knockout mice before and after induction of contact hypersensitivity</CENTER_PROJECT_NAME>
      <STUDY_DESCRIPTION>CD1d-dependent natural killer T (CD1d-NKT) cells play a prominent role in down-regulating aggravated reactions of contact hypersensitivity (CHS), partly through stimulation of IL-10 producing Bregs and possibly mediated via alterations of gut microbiota (GM) composition. We characterized the GM composition (high-throughput 16S rRNA gene-amplicon sequencing) of CD1d knockout (CD1d-KO) and wild-type (Wt) mice before and after contact with contact-allergen-exposure (dinitrochlorobenzene [DNCB]). Prior to CHS induction, we demonstrate that absence of CD1d-NKT cells simultaneously promote (e.g. YS2 bacteria) and limit (e.g. Butyricimonas and an unclassified genus of the Enterobacteriaceae) the presence of rare bacterial members. Further, CD1d-KO tended to harbor a more diverse GM compared to Wt. Upon induction,  the relative abundance of genera belonging to Clostridiales and Bacteroidales  increased in CD1d KO mice, as compared to their Wt littermates. These observations could implicate that changes in GM distribution driven by CD1d-NKT towards a hypersensitivity-tolerance composition may conform a regulatory mechanism for stimulation of IL-10 producing Bregs, which could further help to counteract aggravated reactions of CHS.</STUDY_DESCRIPTION>
    </DESCRIPTOR>
  </STUDY>
</STUDY_SET>
