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Article ; Online: From intestinal stem cells to inflammatory bowel diseases.

Gersemann, Michael / Stange, Eduard Friedrich / Wehkamp, Jan

2011 Volume 17, Issue 27, Page(s) 3198–3203

Abstract: The pathogenesis of both entities of inflammatory bowel disease (IBD), namely Crohn's disease (CD) and ulcerative colitis (UC), is still complex and under investigation. The importance of the microbial flora in developing IBD is beyond debate. In the ... ...

Abstract	The pathogenesis of both entities of inflammatory bowel disease (IBD), namely Crohn's disease (CD) and ulcerative colitis (UC), is still complex and under investigation. The importance of the microbial flora in developing IBD is beyond debate. In the last few years, the focus has changed from adaptive towards innate immunity. Crohn's ileitis is associated with a deficiency of the antimicrobial shield, as shown by a reduced expression and secretion of the Paneth cell defensin HD5 and HD6, which is related to a Paneth cell differentiation defect mediated by a diminished expression of the Wnt transcription factor TCF4. In UC, the protective mucus layer, acting as a physical and chemical barrier between the gut epithelium and the luminal microbes, is thinner and in part denuded as compared to controls. This could be caused by a missing induction of the goblet cell differentiation factors Hath1 and KLF4 leading to immature goblet cells. This defective Paneth and goblet cell differentiation in Crohn's ileitis and UC may enable the luminal microbes to invade the mucosa and trigger the inflammation. The exact molecular mechanisms behind ileal CD and also UC must be further clarified, but these observations could give rise to new therapeutic strategies based on a stimulation of the protective innate immune system.
MeSH term(s)	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Cell Differentiation ; Colitis, Ulcerative/diagnosis ; Crohn Disease/diagnosis ; Goblet Cells/cytology ; Humans ; Inflammatory Bowel Diseases/diagnosis ; Inflammatory Bowel Diseases/pathology ; Intestinal Mucosa/pathology ; Intestines/cytology ; Kruppel-Like Transcription Factors/metabolism ; Paneth Cells/pathology ; Stem Cells/cytology ; Transcription Factor 4 ; Transcription Factors/metabolism ; alpha-Defensins/metabolism
Chemical Substances	ATOH1 protein, human ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Basic Helix-Loop-Helix Transcription Factors ; GKLF protein ; Kruppel-Like Transcription Factors ; TCF4 protein, human ; Transcription Factor 4 ; Transcription Factors ; alpha-Defensins
Language	English
Publishing date	2011-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v17.i27.3198
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Article ; Online: From intestinal stem cells to inflammatory bowel diseases

Michael Gersemann / Eduard Friedrich Stange / Jan Wehkamp

World Journal of Gastroenterology, Vol 17, Iss 27, Pp 3198-

2011 Volume 3203

Abstract: The pathogenesis of both entities of inflammatory bowel disease (IBD), namely Crohn’s disease (CD) and ulcerative colitis (UC), is still complex and under investigation. The importance of the microbial flora in developing IBD is beyond debate. In the ... ...

Abstract	The pathogenesis of both entities of inflammatory bowel disease (IBD), namely Crohn’s disease (CD) and ulcerative colitis (UC), is still complex and under investigation. The importance of the microbial flora in developing IBD is beyond debate. In the last few years, the focus has changed from adaptive towards innate immunity. Crohn’s ileitis is associated with a deficiency of the antimicrobial shield, as shown by a reduced expression and secretion of the Paneth cell defensin HD5 and HD6, which is related to a Paneth cell differentiation defect mediated by a diminished expression of the Wnt transcription factor TCF4. In UC, the protective mucus layer, acting as a physical and chemical barrier between the gut epithelium and the luminal microbes, is thinner and in part denuded as compared to controls. This could be caused by a missing induction of the goblet cell differentiation factors Hath1 and KLF4 leading to immature goblet cells. This defective Paneth and goblet cell differentiation in Crohn’s ileitis and UC may enable the luminal microbes to invade the mucosa and trigger the inflammation. The exact molecular mechanisms behind ileal CD and also UC must be further clarified, but these observations could give rise to new therapeutic strategies based on a stimulation of the protective innate immune system.
Keywords	Inflammatory bowel disease ; Paneth cells ; Goblet cells ; Cell differentiation ; TCF4 ; Hath1 ; KLF4 ; Diseases of the digestive system. Gastroenterology ; RC799-869 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Gastroenterology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Baishideng Publishing Group Co., Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Crohn's disease--defect in innate defence.

Gersemann, Michael / Wehkamp, Jan / Fellermann, Klaus / Stange, Eduard Friedrich

World journal of gastroenterology

2008 Volume 14, Issue 36, Page(s) 5499–5503

Abstract: Crohn's disease may principally involve the whole gastrointestinal tract. Most commonly, the inflammation occurs in the small intestine and/or in the colon with stable disease location over the years. The pathogenesis of both disease phenotypes is ... ...

Abstract	Crohn's disease may principally involve the whole gastrointestinal tract. Most commonly, the inflammation occurs in the small intestine and/or in the colon with stable disease location over the years. The pathogenesis of both disease phenotypes is complex, the likely primary defect lies in the innate rather than adaptive immunity, particularly in the chemical antimicrobial barrier of the mucosa. Crohn's ileitis is associated with a reduced expression of the Wnt signalling pathway transcription factor T-cell factor 4 (TCF4), which is regulating Paneth cell differentiation. As a result, the alpha-defensins and principal Paneth cell products HD5 and HD6 are deficiently expressed in ileal disease, independent of current inflammation. In contrast, Crohn's colitis is typically associated with an impaired induction of the beta-defensins HBD2 and HBD3 caused by fewer gene copy numbers in the gene locus of the beta-defensins on chromosome 8. This ileal and colonic defect in innate defence mediated by a deficiency of the protective alpha- and beta-defensins may enable the luminal microbes to invade the mucosa and trigger the inflammation. A better understanding of the exact molecular mechanisms behind ileal and colonic Crohn's disease may give rise to new therapeutic strategies based on a stimulation of the protective innate immune system.
MeSH term(s)	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Colitis, Ulcerative/immunology ; Colon/immunology ; Crohn Disease/immunology ; DNA-Binding Proteins/metabolism ; Humans ; Ileum/immunology ; Immunity, Innate ; Immunity, Mucosal ; Paneth Cells/immunology ; Stem Cells/immunology ; Transcription Factor 4 ; Transcription Factors/metabolism ; alpha-Defensins/deficiency ; beta-Defensins/deficiency ; beta-Defensins/genetics
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; DEFB4A protein, human ; DNA-Binding Proteins ; TCF4 protein, human ; Transcription Factor 4 ; Transcription Factors ; alpha-Defensins ; beta-Defensins
Language	English
Publishing date	2008-09-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.14.5499
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Conference proceedings: First detection of Elafin in the paranasal sinus mucosa by immunohistochemistry

Tesche, Stefan / Gersemann, Michael / Koops, Susan / Münscher, Adrian

2008 , Page(s) 08hno84

Event/congress	79th Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery; Bonn; German Society of Oto-Rhino-Laryngology, Head and Neck Surgery; 2008
Keywords	Medizin, Gesundheit
Publishing date	2008-07-08
Publisher	German Medical Science; Düsseldorf, Köln
Document type	Conference proceedings
Database	German Medical Science

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Article ; Online: Crohns disease-Defect in innate defence

Michael Gersemann, Jan Wehkamp, Klaus Fellermann, Eduard Friedrich Stange

World Journal of Gastroenterology, Vol 14, Iss 36, Pp 5499-

2008 Volume 5503

Abstract: Crohn’s disease may prinicipally involve the whole gastrointestinal tract. Most commonly, the inflammation occurs in the small intestine and/or in the colon with stable disease location over the years. The pathogenesis of both disease phenotypes is ... ...

Abstract	Crohn’s disease may prinicipally involve the whole gastrointestinal tract. Most commonly, the inflammation occurs in the small intestine and/or in the colon with stable disease location over the years. The pathogenesis of both disease phenotypes is complex, the likely primary defect lies in the innate rather than adaptive immunity, particularly in the chemical antimicrobial barrier of the mucosa. Crohn’s ileitis is associated with a reduced expression of the Wnt signalling pathway transcription factor T-cell factor 4 (TCF4), which is regulating Paneth cell differentiation. As a result, the alpha-defensins and principal Paneth cell products HD5 and HD6 are deficiently expressed in ileal disease, independent of current inflammation. In contrast, Crohn’s colitis is typically associated with an impaired induction of the beta-defensins HBD2 and HBD3 caused by fewer gene copy numbers in the gene locus of the beta-defensins on chromosome 8. This ileal and colonic defect in innate defence mediated by a deficiency of the protective alpha- and beta-defensins may enable the luminal microbes to invade the mucosa and trigger the inflammation. A better understanding of the exact molecular mechanisms behind ileal and colonic Crohn’s disease may give rise to new therapeutic strategies based on a stimulation of the protective innate immune system.
Keywords	Crohn’s disease ; Intestinal stem cell ; Differentiation ; Defensins ; Transcription factor T-cell factor 4 ; Diseases of the digestive system. Gastroenterology ; RC799-869 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Gastroenterology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2008-09-01T00:00:00Z
Publisher	Baishideng Publishing Group Co. Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Conference proceedings: Erster Nachweis der epithelialen Antiprotease Elafin in NNH-Schleimhaut bei chronischer Sinusitis (CRS) mittels Immunhistochemie

Tesche, Stefan / Gersemann, Michael / Koops, Susann / Münscher, Adrian

2008 , Page(s) 08hnod591

Event/congress	79. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; Bonn; Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 2008
Keywords	Medizin, Gesundheit
Publishing date	2008-04-22
Publisher	German Medical Science GMS Publishing House; Düsseldorf
Document type	Conference proceedings
Database	German Medical Science

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Article ; Online: Human colonic mucus is a reservoir for antimicrobial peptides.

Antoni, Lena / Nuding, Sabine / Weller, Dagmar / Gersemann, Michael / Ott, German / Wehkamp, Jan / Stange, Eduard F

Journal of Crohn's & colitis

2013 Volume 7, Issue 12, Page(s) e652–64

Abstract: Background and aims: To prevent bacterial adherence and translocation, the colonic mucosa is covered by a protecting mucus layer and the epithelium synthesizes antimicrobial peptides. The present qualitative study investigated the contents and ... ...

Abstract	Background and aims: To prevent bacterial adherence and translocation, the colonic mucosa is covered by a protecting mucus layer and the epithelium synthesizes antimicrobial peptides. The present qualitative study investigated the contents and interaction of these peptides in and with rectal mucus. Methods: Rectal mucus extracts were analyzed for antimicrobial activity and screened with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, Dot blot and immunohistochemistry for antimicrobial peptides. In addition, binding of AMPs to mucins was investigated by Western blot and enzyme-linked lectin assays. Results: In functional tests the mucus layer exhibited a strong antimicrobial activity. We detected 11 antimicrobial peptides in mucus extracts from healthy persons including the defensins HBD-1 and -3, the cathelicidin LL-37, ubiquitin, lysozyme, histones, high mobility group nucleosome-binding domain-containing protein 2, ubiquicidin and other ribosomal proteins. AMPs were bound by mucins but this was demonstrated to be reversible and inhibition of antibacterial activity was limited. Conclusion: These findings indicate that epithelial antimicrobial peptides are retained in the intestinal mucus layer without losing their efficacy. Thus, the mucus layer and its composition provide an attractive drug target to restore antimicrobial barrier function in intestinal diseases.
MeSH term(s)	Anti-Infective Agents/analysis ; Bacteroides fragilis/growth & development ; Candida albicans/growth & development ; Cathelicidins/analysis ; Cathelicidins/metabolism ; Defensins/analysis ; Defensins/metabolism ; Enterococcus faecalis/growth & development ; Escherichia coli/growth & development ; Flow Cytometry ; HMGN2 Protein/analysis ; HMGN2 Protein/metabolism ; Histones/analysis ; Histones/metabolism ; Humans ; Intestinal Mucosa/chemistry ; Microbial Sensitivity Tests ; Mucins/metabolism ; Mucus/chemistry ; Mucus/metabolism ; Muramidase/analysis ; Muramidase/metabolism ; Peptides/analysis ; Peptides/metabolism ; Rectum/chemistry ; Ribosomal Proteins/analysis ; Ribosomal Proteins/metabolism ; Staphylococcus aureus/growth & development ; Ubiquitin/analysis ; Ubiquitin/metabolism
Chemical Substances	Anti-Infective Agents ; Cathelicidins ; Defensins ; HMGN2 Protein ; Histones ; Mucins ; Peptides ; Ribosomal Proteins ; Ubiquitin ; ribosomal protein S30 ; Muramidase (EC 3.2.1.17)
Language	English
Publishing date	2013-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2390120-2
ISSN	1876-4479 ; 1873-9946
ISSN (online)	1876-4479
ISSN	1873-9946
DOI	10.1016/j.crohns.2013.05.006
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Article ; Online: Bacteria regulate intestinal epithelial cell differentiation factors both in vitro and in vivo.

Becker, Svetlana / Oelschlaeger, Tobias A / Wullaert, Andy / Vlantis, Katerina / Pasparakis, Manolis / Wehkamp, Jan / Stange, Eduard F / Gersemann, Michael

PloS one

2013 Volume 8, Issue 2, Page(s) e55620

Abstract: Background: The human colon harbours a plethora of bacteria known to broadly impact on mucosal metabolism and function and thought to be involved in inflammatory bowel disease pathogenesis and colon cancer development. In this report, we investigated ... ...

Abstract	Background: The human colon harbours a plethora of bacteria known to broadly impact on mucosal metabolism and function and thought to be involved in inflammatory bowel disease pathogenesis and colon cancer development. In this report, we investigated the effect of colonic bacteria on epithelial cell differentiation factors in vitro and in vivo. As key transcription factors we focused on Hes1, known to direct towards an absorptive cell fate, Hath1 and KLF4, which govern goblet cell. Methods: Expression of the transcription factors Hes1, Hath1 and KLF4, the mucins Muc1 and Muc2 and the defensin HBD2 were measured by real-time PCR in LS174T cells following incubation with several heat-inactivated E. coli strains, including the probiotic E. coli Nissle 1917+/- flagellin, Lactobacilli and Bifidobacteria. For protein detection Western blot experiments and chamber-slide immunostaining were performed. Finally, mRNA and protein expression of these factors was evaluated in the colon of germfree vs. specific pathogen free vs. conventionalized mice and colonic goblet cells were counted. Results: Expression of Hes1 and Hath1, and to a minor degree also of KLF4, was reduced by E. coli K-12 and E. coli Nissle 1917. In contrast, Muc1 and HBD2 expression were significantly enhanced, independent of the Notch signalling pathway. Probiotic E. coli Nissle 1917 regulated Hes1, Hath1, Muc1 and HBD2 through flagellin. In vivo experiments confirmed the observed in vitro effects of bacteria by a diminished colonic expression of Hath1 and KLF4 in specific pathogen free and conventionalized mice as compared to germ free mice whereas the number of goblet cells was unchanged in these mice. Conclusions: Intestinal bacteria influence the intestinal epithelial differentiation factors Hes1, Hath1 and KLF4, as well as Muc1 and HBD2, in vitro and in vivo. The induction of Muc1 and HBD2 seems to be triggered directly by bacteria and not by Notch.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Bifidobacterium ; Cell Differentiation/physiology ; Cell Line, Tumor ; Colon/cytology ; Colon/metabolism ; Colon/microbiology ; Escherichia coli ; Goblet Cells/cytology ; Goblet Cells/metabolism ; Goblet Cells/microbiology ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Lactobacillus ; Mice ; Mice, Inbred C57BL ; Mucin-1/genetics ; Mucin-1/metabolism ; Mucin-2/genetics ; Mucin-2/metabolism ; Transcription Factor HES-1 ; beta-Defensins/genetics ; beta-Defensins/metabolism
Chemical Substances	ATOH1 protein, human ; Basic Helix-Loop-Helix Transcription Factors ; DEFB4A protein, human ; GKLF protein ; Homeodomain Proteins ; Kruppel-Like Transcription Factors ; MUC1 protein, human ; MUC2 protein, human ; Mucin-1 ; Mucin-2 ; Transcription Factor HES-1 ; beta-Defensins ; HES1 protein, human (149348-15-2)
Language	English
Publishing date	2013-02-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0055620
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Article ; Online: Correction

Svetlana Becker / Tobias A. Oelschlaeger / Andy Wullaert / Katerina Vlantis / Manolis Pasparakis / Jan Wehkamp / Eduard F. Stange / Michael Gersemann

PLoS ONE, Vol 8, Iss

Bacteria Regulate Intestinal Epithelial Cell Differentiation Factors Both and.

2013 Volume 5

Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: TCF-1-mediated Wnt signaling regulates Paneth cell innate immune defense effectors HD-5 and -6: implications for Crohn's disease.

Beisner, Julia / Teltschik, Zora / Ostaff, Maureen J / Tiemessen, Machteld M / Staal, Frank J T / Wang, Guoxing / Gersemann, Michael / Perminow, Gori / Vatn, Morten H / Schwab, Matthias / Stange, Eduard F / Wehkamp, Jan

American journal of physiology. Gastrointestinal and liver physiology

2014 Volume 307, Issue 5, Page(s) G487–98

Abstract: Wnt signaling regulates small intestinal stem cell maintenance and Paneth cell differentiation. In patients with ileal Crohn's disease (CD), a decrease of Paneth cell α-defensins has been observed that is partially caused by impaired TCF-4 and LRP6 ... ...

Abstract	Wnt signaling regulates small intestinal stem cell maintenance and Paneth cell differentiation. In patients with ileal Crohn's disease (CD), a decrease of Paneth cell α-defensins has been observed that is partially caused by impaired TCF-4 and LRP6 function. Here we show reduced expression of the Wnt signaling effector TCF-1 (also known as TCF-7) in patients with ileal CD. Reporter gene assays and in vitro promoter binding analysis revealed that TCF-1 activates α-defensin HD-5 and HD-6 transcription in cooperation with β-catenin and that activation is mediated by three distinct TCF binding sites. EMSA analysis showed binding of TCF-1 to the respective motifs. In ileal CD patients, TCF-1 mRNA expression levels were significantly reduced. Moreover, we found specifically reduced expression of active TCF-1 mRNA isoforms. Tcf-1 knockout mice exhibited reduced cryptdin expression in the jejunum, which was not consistently seen at other small intestinal locations. Our data provide evidence that TCF-1-mediated Wnt signaling is disturbed in small intestinal CD, which might contribute to the observed barrier dysfunction in the disease.
MeSH term(s)	Adolescent ; Animals ; Binding Sites ; Caco-2 Cells ; Crohn Disease/metabolism ; Female ; HEK293 Cells ; Humans ; Ileum/metabolism ; Ileum/pathology ; Jejunum/metabolism ; Jejunum/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Organ Specificity ; Paneth Cells/metabolism ; Protein Precursors/genetics ; Protein Precursors/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; T Cell Transcription Factor 1/chemistry ; T Cell Transcription Factor 1/genetics ; T Cell Transcription Factor 1/metabolism ; Wnt Signaling Pathway ; alpha-Defensins/genetics ; alpha-Defensins/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	Protein Precursors ; RNA, Messenger ; T Cell Transcription Factor 1 ; alpha-Defensins ; beta Catenin ; cryptdin (120668-29-3)
Language	English
Publishing date	2014-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00347.2013
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