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  1. Article ; Online: Modulation of intestinal IL-37 expression and its impact on the epithelial innate immune response and barrier integrity.

    Kröhn, Laura / Azabdaftari, Aline / Heuberger, Julian / Hudert, Christian / Zilbauer, Matthias / Breiderhoff, Tilman / Bufler, Philip

    Frontiers in immunology

    2023  Volume 14, Page(s) 1261666

    Abstract: Background and aims: Intestinal epithelial cells separate the luminal flora from lamina propria immune cells and regulate innate immune responses in the gut. An imbalance of the mucosal immune response and disrupted intestinal barrier integrity ... ...

    Abstract Background and aims: Intestinal epithelial cells separate the luminal flora from lamina propria immune cells and regulate innate immune responses in the gut. An imbalance of the mucosal immune response and disrupted intestinal barrier integrity contribute to the evolution of inflammatory bowel diseases. Interleukin (IL)-37 has broad anti- inflammatory activity and is expressed by the human intestinal epithelium. Mice ectopically expressing human IL-37 show reduced epithelial damage and inflammation after DSS-induced colitis. Here, we investigated the impact of IL-37 on the innate immune response and tight junction protein expression of mouse intestinal organoids and the modulation of
    Methods: Murine intestinal organoids were generated from IL-37tg and wildtype mice. Human ileal organoids were generated from healthy young donors.
    Results: Expression of transgene IL-37 or recombinant IL-37 protein did not significantly reduce overall proinflammatory cytokine mRNA expression in murine intestinal organoids. However, higher
    Conclusions: We speculate that the anti-inflammatory activity of IL-37 in the intestine is mainly mediated by lamina propria immune cells protecting intestinal epithelial integrity.
    MeSH term(s) Humans ; Mice ; Animals ; Tumor Necrosis Factor-alpha/metabolism ; Intestinal Mucosa ; Immunity, Innate ; Cytokines/metabolism ; RNA, Messenger/metabolism ; Interleukin-1/genetics ; Interleukin-1/metabolism
    Chemical Substances Tumor Necrosis Factor-alpha ; Cytokines ; RNA, Messenger ; IL37 protein, human ; Interleukin-1
    Language English
    Publishing date 2023-09-20
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1261666
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Thesis: Shp2 reguliert die Differenzierung intestinaler Epithelzellen

    Heuberger, Julian

    2012  

    Author's details von Julian Heuberger
    Language German
    Size 2 Mikrofiches, Ill., graph. Darst.
    Document type Book ; Thesis
    Thesis / German Habilitation thesis @Berlin, Humboldt-Univ., Diss., 2012
    Database Special collection on veterinary medicine and general parasitology

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  3. Book ; Thesis: Shp2 reguliert die Differenzierung intestinaler Epithelzellen

    Heuberger, Julian

    2012  

    Author's details von Julian Heuberger
    Language German
    Size 2 Mikrofiches, Ill., graph. Darst.
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Humboldt-Univ., Diss.--Berlin, 2012
    Database Former special subject collection: coastal and deep sea fishing

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  4. Conference proceedings ; Online: Impact of Access Barring Schemes for Delay Tolerant MTC Devices on Energy Consumption

    Popp, Julian / Robert, Jörg / Roth-Mandutz, Elke / Heuberger, Albert

    2022  

    Abstract: 3163 ... 3168 ... Cellular mobile communication systems have evolved from voice-centric to universal communication systems. After release 10 of the 3GPP standard, the group started working on specific enhancements tailored for machine-type communication (MTC) ...

    Abstract 3163

    3168

    Cellular mobile communication systems have evolved from voice-centric to universal communication systems. After release 10 of the 3GPP standard, the group started working on specific enhancements tailored for machine-type communication (MTC), e.g. improving energy consumption, coverage enhancements and support for massive number of devices per cell. During the study for MTC enhancements, congestion on the random access channel was identified as a major issue in case a very high number of MTC devices tries to simultaneously access the cell. The existing access class barring (ACB) is a threshold based approach affecting all devices in a cell. Thus a new barring mechanism for latency-tolerant MTC devices was introduced: enhanced access barring (EAB). There have been numerous publications in the last years on how to optimize ACB and EAB for throughput and latency but only very few considered the major important impact on the overall energy consumption of the devices. Unlike previous publications, this paper investigates the effect of different access barring schemes on the energy consumption of MTC devices in case of high load on the random access channel and compares static and dynamic ACB settings as well as EAB-based solutions.
    Keywords 3GPP ; 5G ; ACB ; Access Barring ; Congestion Control ; EAB ; Energy Consumption ; IoT ; MTC
    Subject code 306
    Language English
    Publishing country de
    Document type Conference proceedings ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Epigenetic modifier balances Mapk and Wnt signalling in differentiation of goblet and Paneth cells.

    Grinat, Johanna / Kosel, Frauke / Goveas, Neha / Kranz, Andrea / Alexopoulou, Dimitra / Rajewsky, Klaus / Sigal, Michael / Stewart, A Francis / Heuberger, Julian

    Life science alliance

    2022  Volume 5, Issue 4

    Abstract: Differentiation and lineage specification are controlled by cooperation of growth factor signalling. The involvement of epigenetic regulators in lineage specification remains largely elusive. Here, we show that the histone methyltransferase Mll1 prevents ...

    Abstract Differentiation and lineage specification are controlled by cooperation of growth factor signalling. The involvement of epigenetic regulators in lineage specification remains largely elusive. Here, we show that the histone methyltransferase Mll1 prevents intestinal progenitor cells from differentiation, whereas it is also involved in secretory lineage specification of Paneth and goblet cells. Using conditional mutagenesis in mice and intestinal organoids, we demonstrate that loss of Mll1 renders intestinal progenitor cells permissive for Wnt-driven secretory differentiation. However, Mll1-deficient crypt cells fail to segregate Paneth and goblet cell fates. Mll1 deficiency causes Paneth cell-determined crypt progenitors to exhibit goblet cell features by unleashing Mapk signalling, resulting in increased numbers of mixed Paneth/goblet cells. We show that loss of Mll1 abolishes the pro-proliferative effect of Mapk signalling in intestinal progenitor cells and promotes Mapk-induced goblet cell differentiation. Our data uncover Mll1 and its downstream targets Gata4/6 as a regulatory hub of Wnt and Mapk signalling in the control of lineage specification of intestinal secretory Paneth and goblet cells.
    MeSH term(s) Animals ; Cell Differentiation/genetics ; Epigenesis, Genetic/genetics ; Epigenomics/methods ; Female ; Goblet Cells/cytology ; Goblet Cells/metabolism ; Humans ; Intestinal Mucosa/metabolism ; Intestines ; MAP Kinase Signaling System/genetics ; MAP Kinase Signaling System/physiology ; Male ; Mice ; Mice, Transgenic ; Organoids/metabolism ; Paneth Cells/cytology ; Paneth Cells/metabolism ; Stem Cells/metabolism ; Wnt Signaling Pathway/genetics ; Wnt Signaling Pathway/physiology
    Language English
    Publishing date 2022-01-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.202101187
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Establishment of gastrointestinal assembloids to study the interplay between epithelial crypts and their mesenchymal niche.

    Lin, Manqiang / Hartl, Kimberly / Heuberger, Julian / Beccaceci, Giulia / Berger, Hilmar / Li, Hao / Liu, Lichao / Müllerke, Stefanie / Conrad, Thomas / Heymann, Felix / Woehler, Andrew / Tacke, Frank / Rajewsky, Nikolaus / Sigal, Michael

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 3025

    Abstract: The cellular organization of gastrointestinal crypts is orchestrated by different cells of the stromal niche but available in vitro models fail to fully recapitulate the interplay between epithelium and stroma. Here, we establish a colon assembloid ... ...

    Abstract The cellular organization of gastrointestinal crypts is orchestrated by different cells of the stromal niche but available in vitro models fail to fully recapitulate the interplay between epithelium and stroma. Here, we establish a colon assembloid system comprising the epithelium and diverse stromal cell subtypes. These assembloids recapitulate the development of mature crypts resembling in vivo cellular diversity and organization, including maintenance of a stem/progenitor cell compartment in the base and their maturation into secretory/absorptive cell types. This process is supported by self-organizing stromal cells around the crypts that resemble in vivo organization, with cell types that support stem cell turnover adjacent to the stem cell compartment. Assembloids that lack BMP receptors either in epithelial or stromal cells fail to undergo proper crypt formation. Our data highlight the crucial role of bidirectional signaling between epithelium and stroma, with BMP as a central determinant of compartmentalization along the crypt axis.
    MeSH term(s) Cell Differentiation ; Intestinal Mucosa/metabolism ; Gastrointestinal Tract ; Signal Transduction ; Stem Cells/metabolism
    Language English
    Publishing date 2023-05-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-38780-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Establishment of gastrointestinal assembloids to study the interplay between epithelial crypts and their mesenchymal niche

    Manqiang Lin / Kimberly Hartl / Julian Heuberger / Giulia Beccaceci / Hilmar Berger / Hao Li / Lichao Liu / Stefanie Müllerke / Thomas Conrad / Felix Heymann / Andrew Woehler / Frank Tacke / Nikolaus Rajewsky / Michael Sigal

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 14

    Abstract: Abstract The cellular organization of gastrointestinal crypts is orchestrated by different cells of the stromal niche but available in vitro models fail to fully recapitulate the interplay between epithelium and stroma. Here, we establish a colon ... ...

    Abstract Abstract The cellular organization of gastrointestinal crypts is orchestrated by different cells of the stromal niche but available in vitro models fail to fully recapitulate the interplay between epithelium and stroma. Here, we establish a colon assembloid system comprising the epithelium and diverse stromal cell subtypes. These assembloids recapitulate the development of mature crypts resembling in vivo cellular diversity and organization, including maintenance of a stem/progenitor cell compartment in the base and their maturation into secretory/absorptive cell types. This process is supported by self-organizing stromal cells around the crypts that resemble in vivo organization, with cell types that support stem cell turnover adjacent to the stem cell compartment. Assembloids that lack BMP receptors either in epithelial or stromal cells fail to undergo proper crypt formation. Our data highlight the crucial role of bidirectional signaling between epithelium and stroma, with BMP as a central determinant of compartmentalization along the crypt axis.
    Keywords Science ; Q
    Subject code 571
    Language English
    Publishing date 2023-05-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Genomic aberrations after short-term exposure to colibactin-producing E. coli transform primary colon epithelial cells.

    Iftekhar, Amina / Berger, Hilmar / Bouznad, Nassim / Heuberger, Julian / Boccellato, Francesco / Dobrindt, Ulrich / Hermeking, Heiko / Sigal, Michael / Meyer, Thomas F

    Nature communications

    2021  Volume 12, Issue 1, Page(s) 1003

    Abstract: Genotoxic colibactin-producing pks+ Escherichia coli induce DNA double-strand breaks, mutations, and promote tumor development in mouse models of colorectal cancer (CRC). Colibactin's distinct mutational signature is reflected in human CRC, suggesting a ... ...

    Abstract Genotoxic colibactin-producing pks+ Escherichia coli induce DNA double-strand breaks, mutations, and promote tumor development in mouse models of colorectal cancer (CRC). Colibactin's distinct mutational signature is reflected in human CRC, suggesting a causal link. Here, we investigate its transformation potential using organoids from primary murine colon epithelial cells. Organoids recovered from short-term infection with pks+ E. coli show characteristics of CRC cells, e.g., enhanced proliferation, Wnt-independence, and impaired differentiation. Sequence analysis of Wnt-independent organoids reveals an enhanced mutational burden, including chromosomal aberrations typical of genomic instability. Although we do not find classic Wnt-signaling mutations, we identify several mutations in genes related to p53-signaling, including miR-34a. Knockout of Trp53 or miR-34 in organoids results in Wnt-independence, corroborating a functional interplay between the p53 and Wnt pathways. We propose larger chromosomal alterations and aneuploidy as the basis of transformation in these organoids, consistent with the early appearance of chromosomal instability in CRC.
    MeSH term(s) Animals ; Chromosome Aberrations ; Colon/pathology ; Colonic Neoplasms/genetics ; Colonic Neoplasms/pathology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/psychology ; DNA Damage ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Genomics ; Male ; Mice ; Mice, Knockout ; Mutation ; Organoids ; Peptides/genetics ; Peptides/metabolism ; Polyketides/metabolism
    Chemical Substances Peptides ; Polyketides ; colibactin
    Language English
    Publishing date 2021-02-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-21162-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Genomic aberrations after short-term exposure to colibactin-producing E. coli transform primary colon epithelial cells

    Amina Iftekhar / Hilmar Berger / Nassim Bouznad / Julian Heuberger / Francesco Boccellato / Ulrich Dobrindt / Heiko Hermeking / Michael Sigal / Thomas F. Meyer

    Nature Communications, Vol 12, Iss 1, Pp 1-

    2021  Volume 15

    Abstract: Colibactin-producing pks+ Escherichia coli are frequent constituents of the human intestinal microbiota. Here, the authors show that short exposure of cells to pks+ E. coli induces chromosomal aberrations, genomic instability, and multiple features of ... ...

    Abstract Colibactin-producing pks+ Escherichia coli are frequent constituents of the human intestinal microbiota. Here, the authors show that short exposure of cells to pks+ E. coli induces chromosomal aberrations, genomic instability, and multiple features of transformation reminiscent of colorectal cancer.
    Keywords Science ; Q
    Language English
    Publishing date 2021-02-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
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  10. Article ; Online: R-spondin/YAP axis promotes gastric oxyntic gland regeneration and Helicobacter pylori-associated metaplasia in mice.

    Fischer, Anne-Sophie / Müllerke, Stefanie / Arnold, Alexander / Heuberger, Julian / Berger, Hilmar / Lin, Manqiang / Mollenkopf, Hans-Joachim / Wizenty, Jonas / Horst, David / Tacke, Frank / Sigal, Michael

    The Journal of clinical investigation

    2022  Volume 132, Issue 21

    Abstract: The stomach corpus epithelium is organized into anatomical units that consist of glands and pits. Mechanisms that control the cellular organization of corpus glands and enable their recovery upon injury are not well understood. R-spondin 3 (RSPO3) is a ... ...

    Abstract The stomach corpus epithelium is organized into anatomical units that consist of glands and pits. Mechanisms that control the cellular organization of corpus glands and enable their recovery upon injury are not well understood. R-spondin 3 (RSPO3) is a WNT-signaling enhancer that regulates stem cell behavior in different organs. Here, we investigated the function of RSPO3 in the corpus during homeostasis, upon chief and/or parietal cell loss, and during chronic Helicobacter pylori infection. Using organoid culture and conditional mouse models, we demonstrate that RSPO3 is a critical driver of secretory cell differentiation in the corpus gland toward parietal and chief cells, while its absence promoted pit cell differentiation. Acute loss of chief and parietal cells induced by high dose tamoxifen - or merely the depletion of LGR5+ chief cells - caused an upregulation of RSPO3 expression, which was required for the initiation of a coordinated regenerative response via the activation of yes-associated protein (YAP) signaling. This response enabled a rapid recovery of the injured secretory gland cells. However, in the context of chronic H. pylori infection, the R-spondin-driven regeneration was maintained long term, promoting severe glandular hyperproliferation and the development of premalignant metaplasia.
    MeSH term(s) Mice ; Animals ; Helicobacter pylori/metabolism ; Helicobacter Infections/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Gastric Mucosa/metabolism ; Metaplasia/metabolism ; Metaplasia/pathology ; Stomach/pathology ; Regeneration ; Stomach Neoplasms/metabolism
    Chemical Substances Receptors, G-Protein-Coupled
    Language English
    Publishing date 2022-11-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI151363
    Database MEDical Literature Analysis and Retrieval System OnLINE

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