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Article: The Punicalagin Metabolites Ellagic Acid and Urolithin A Exert Different Strengthening and Anti-Inflammatory Effects on Tight Junction-Mediated Intestinal Barrier Function

Hering, Nina A / Luettig, Julia / Jebautzke, Britta / Schulzke, Jörg D / Rosenthal, Rita

2021 Volume 12, Page(s) 610164

Abstract: Scope: ...

Abstract	Scope:
Language	English
Publishing date	2021-03-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2021.610164
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Article ; Online: Hereditary barrier-related diseases involving the tight junction: lessons from skin and intestine.

Brandner, Johanna M / Schulzke, Jörg D

Cell and tissue research

2015 Volume 360, Issue 3, Page(s) 723–748

Abstract: The tight junction (TJ) regulates paracellular barrier properties. TJs are composed of transmembrane proteins, i.e., claudins, occludin, tricellulin and junctional adhesion molecules as well as TJ plaque proteins. Their relative abundance and composition ...

Abstract	The tight junction (TJ) regulates paracellular barrier properties. TJs are composed of transmembrane proteins, i.e., claudins, occludin, tricellulin and junctional adhesion molecules as well as TJ plaque proteins. Their relative abundance and composition determines epithelial tightness. TJs undergo rapid regulation by various signalling pathways, either directly addressing TJ transmembrane proteins or via plaque proteins and the cytoskeleton. In the skin, TJs exert predominantly barrier functions, while in the intestine they also mediate paracellular ion and water transport. In diseases, TJs can either be primarily affected (hereditary TJ defects) or changes can result from secondary regulatory inputs as, e.g., in inflammatory diseases (secondary TJ defects). Secondary TJ defects can maintain disease activity, e.g., by enhanced antigen leak. This review discusses TJ composition, function and regulation as well as primary and secondary tight junction defects in a comparative manner in skin and intestine in order to elucidate similarities and differences.
MeSH term(s)	Animals ; Epithelium/pathology ; Genetic Diseases, Inborn/pathology ; Humans ; Intestinal Diseases ; Intestines/pathology ; Skin/pathology ; Skin Diseases/pathology ; Tight Junctions/pathology
Language	English
Publishing date	2015-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-014-2096-1
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Article ; Online: Human duodenal organoid-derived monolayers serve as a suitable barrier model for duodenal tissue.

Weiß, Franziska / Holthaus, David / Kraft, Martin / Klotz, Christian / Schneemann, Martina / Schulzke, Jörg D / Krug, Susanne M

Annals of the New York Academy of Sciences

2022 Volume 1515, Issue 1, Page(s) 155–167

Abstract: Usually, duodenal barriers are investigated using intestinal cell lines like Caco-2, which in contrast to native tissue are limited in cell-type representation. Organoids can consist of all intestinal cell types and are supposed to better reflect the in ... ...

Abstract	Usually, duodenal barriers are investigated using intestinal cell lines like Caco-2, which in contrast to native tissue are limited in cell-type representation. Organoids can consist of all intestinal cell types and are supposed to better reflect the in vivo situation. Growing three-dimensionally, with the apical side facing the lumen, application of typical physiological techniques to analyze the barrier is difficult. Organoid-derived monolayers (ODMs) were developed to overcome this. After optimizing culturing conditions, ODMs were characterized and compared to Caco-2 and duodenal tissue. Tight junction composition and appearance were analyzed, and electrophysiological barrier properties, like paracellular and transcellular barrier function and macromolecule permeability, were evaluated. Furthermore, transcriptomic data were analyzed. ODMs had tight junction protein expression and paracellular barrier properties much more resembling the originating tissue than Caco-2. Transcellular barrier was similar between ODMs and native tissue but was increased in Caco-2. Transcriptomic data showed that Caco-2 expressed fewer solute carriers than ODMs and native tissue. In conclusion, while Caco-2 cells differ mostly in transcellular properties, ODMs reflect trans- and paracellular properties of the originating tissue. If cultured under optimized conditions, ODMs possess reproducible functionality, and the variety of different cell types makes them a suitable model for human tissue-specific investigations.
MeSH term(s)	Caco-2 Cells ; Humans ; Intestinal Mucosa/metabolism ; Organoids ; Permeability ; Tight Junction Proteins/metabolism ; Tight Junctions/metabolism
Chemical Substances	Tight Junction Proteins
Language	English
Publishing date	2022-06-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/nyas.14804
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Article ; Online: Uptake of

Friebel, Julian / Schinnerling, Katina / Weigt, Kathleen / Heldt, Claudia / Fromm, Anja / Bojarski, Christian / Siegmund, Britta / Epple, Hans-Jörg / Kikhney, Judith / Moter, Annette / Schneider, Thomas / Schulzke, Jörg D / Moos, Verena / Schumann, Michael

International journal of molecular sciences

2023 Volume 24, Issue 7

Abstract: Background: Tropheryma whipplei: Methods: Using ex vivo disease models comprising human duodenal mucosa exposed to : Results: TW: Conclusions: ... ...

Abstract	Background: Tropheryma whipplei Methods: Using ex vivo disease models comprising human duodenal mucosa exposed to Results: TW Conclusions: TW
MeSH term(s)	Humans ; Tropheryma/physiology ; Actins/metabolism ; Macrophages/microbiology ; Intestinal Mucosa/metabolism ; Gastroenteritis/microbiology
Chemical Substances	Actins
Language	English
Publishing date	2023-03-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24076197
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Article ; Online: Tricellulin Effect on Paracellular Water Transport.

Ayala-Torres, Carlos / Krug, Susanne M / Schulzke, Jörg D / Rosenthal, Rita / Fromm, Michael

International journal of molecular sciences

2019 Volume 20, Issue 22

Abstract: In epithelia, large amounts of water pass by transcellular and paracellular pathways, driven by the osmotic gradient built up by the movement of solutes. The transcellular pathway has been molecularly characterized by the discovery of aquaporin membrane ... ...

Abstract	In epithelia, large amounts of water pass by transcellular and paracellular pathways, driven by the osmotic gradient built up by the movement of solutes. The transcellular pathway has been molecularly characterized by the discovery of aquaporin membrane channels. Unlike this, the existence of a paracellular pathway for water through the tight junctions (TJ) was discussed controversially for many years until two molecular components of paracellular water transport, claudin-2 and claudin-15, were identified. A main protein of the tricellular TJ (tTJ), tricellulin, was shown to be downregulated in ulcerative colitis leading to increased permeability to macromolecules. Whether or not tricellulin also regulates water transport is unknown yet. To this end, an epithelial cell line featuring properties of a tight epithelium, Madin-Darby canine kidney cells clone 7 (MDCK C7), was stably transfected with small hairpin RNA (shRNA) targeting tricellulin, a protein of the tTJ essential for the barrier against passage of solutes up to 10 kDa. Water flux was induced by osmotic gradients using mannitol or 4 and 40 kDa-dextran. Water flux in tricellulin knockdown (KD) cells was higher compared to that of vector controls, indicating a direct role of tricellulin in regulating water permeability in a tight epithelial cell line. We conclude that tricellulin increases water permeability at reduced expression.
MeSH term(s)	Animals ; Biological Transport ; Cell Line ; Cell Membrane Permeability ; Dogs ; Epithelium/metabolism ; Gene Knockdown Techniques ; MARVEL Domain Containing 2 Protein/genetics ; MARVEL Domain Containing 2 Protein/metabolism ; Madin Darby Canine Kidney Cells ; Tight Junctions/metabolism ; Water/metabolism
Chemical Substances	MARVEL Domain Containing 2 Protein ; Water (059QF0KO0R)
Language	English
Publishing date	2019-11-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20225700
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Article ; Online: Phospholipid effects on SGLT1-mediated glucose transport in rabbit ileum brush border membrane vesicles.

Ebel, Hans / Fromm, Anja / Günzel, Dorothee / Fromm, Michael / Schulzke, Jörg D

Biochimica et biophysica acta. Biomembranes

2019 Volume 1861, Issue 10, Page(s) 182985

Abstract: In small intestine, sodium-glucose cotransporter SGLT1 provides the main mechanism for sugar uptake. We investigated the effect of membrane phospholipids (PL) on this transport in rabbit ileal brush border membrane vesicles (BBMV). For this, PL of ... ...

Abstract	In small intestine, sodium-glucose cotransporter SGLT1 provides the main mechanism for sugar uptake. We investigated the effect of membrane phospholipids (PL) on this transport in rabbit ileal brush border membrane vesicles (BBMV). For this, PL of different charge, length, and saturation were incorporated into BBMV. Transport was measured related to (i) membrane surface charge (membrane-bound MC540 fluorescence), (ii) membrane thickness (PL incorporation of different acyl chain length), and (iii) membrane fluidity (r
MeSH term(s)	Animals ; Biological Transport ; Fatty Acids/metabolism ; Fluorescence Polarization/methods ; Glucose/metabolism ; Glucose Transport Proteins, Facilitative/metabolism ; Glucose Transport Proteins, Facilitative/physiology ; Ileum/metabolism ; Intestine, Small/metabolism ; Male ; Membrane Fluidity/drug effects ; Microvilli/metabolism ; Microvilli/physiology ; Phosphatidic Acids/chemistry ; Phosphatidylcholines/chemistry ; Phosphatidylinositols/chemistry ; Phospholipids/metabolism ; Phospholipids/physiology ; Rabbits ; Sodium/metabolism ; Sodium-Glucose Transporter 1/metabolism ; Sodium-Glucose Transporter 1/physiology ; Transport Vesicles/metabolism ; Transport Vesicles/physiology
Chemical Substances	Fatty Acids ; Glucose Transport Proteins, Facilitative ; Phosphatidic Acids ; Phosphatidylcholines ; Phosphatidylinositols ; Phospholipids ; Sodium-Glucose Transporter 1 ; Sodium (9NEZ333N27) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-05-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-2642 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2642 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamem.2019.05.007
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Article ; Online: Zinc strengthens the jejunal barrier by reversibly tightening the paracellular route.

Zakrzewski, Silke S / Fromm, Michael / Schulzke, Joerg D / Günzel, Dorothee

American journal of physiology. Gastrointestinal and liver physiology

2017 , Page(s) ajpgi.00355.2016

Abstract: During the post weaning period, piglets are prone to gastrointestinal infections. The resulting impairment of intestinal barrier function may cause diarrhea associated with growth retardation or even death of piglets. Orally applied zinc is commonly used ...

Abstract	During the post weaning period, piglets are prone to gastrointestinal infections. The resulting impairment of intestinal barrier function may cause diarrhea associated with growth retardation or even death of piglets. Orally applied zinc is commonly used to prevent and treat diarrhea but its mode of action still needs to be elucidated. In order to analyze the molecular mechanism whereby zinc acts on porcine intestinal barrier function, ex vivo studies on piglet jejunum and accompanying in vitro studies on a porcine jejunal epithelial cell line, IPEC-J2/PS, were performed with electrophysiological tools. Feeding pharmacological zinc doses exerted no significant electrophysiologically ascertainable short- and long-term effects on jejunal barrier function ex vivo. However, in IPEC-J2/PS, basolateral zinc was cytotoxic since its application caused a release of lactate dehydrogenase and an irreversible break-down of the epithelial barrier. In contrast, apical zinc application caused an immediate increase in paracellular resistance and a decrease in permeability to the paracellular marker fluorescein, reflecting overall barrier strengthening in vitro. Apical effects were fully reversible upon wash-out. This indicates that zinc supplemented to feed was completely washed out during ex vivo jejunum preparation. We conclude that there is no evidence for long-term barrier effects through prophylactic zinc supplementation and that extracellular zinc acts acutely and reversibly from the apical side via tightening the paracellular route, thus counteracting leak-flux diarrhea.
Language	English
Publishing date	2017-09-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00355.2016
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Article: Celiac Disease: Role of the Epithelial Barrier.

Schumann, Michael / Siegmund, Britta / Schulzke, Jörg D / Fromm, Michael

Cellular and molecular gastroenterology and hepatology

2017 Volume 3, Issue 2, Page(s) 150–162

Abstract: In celiac disease (CD) a T-cell-mediated response to gluten is mounted in genetically predisposed individuals, resulting in a malabsorptive enteropathy histologically highlighted by villous atrophy and crypt hyperplasia. Recent data point to the ... ...

Abstract	In celiac disease (CD) a T-cell-mediated response to gluten is mounted in genetically predisposed individuals, resulting in a malabsorptive enteropathy histologically highlighted by villous atrophy and crypt hyperplasia. Recent data point to the epithelial layer as an under-rated hot spot in celiac pathophysiology to date. This overview summarizes current functional and genetic evidence on the role of the epithelial barrier in CD, consisting of the cell membranes and the apical junctional complex comprising sealing as well as ion and water channel-forming tight junction proteins and the adherens junction. Moreover, the underlying mechanisms are discussed, including apoptosis of intestinal epithelial cells, biology of intestinal stem cells, alterations in the apical junctional complex, transcytotic uptake of gluten peptides, and possible implications of a defective epithelial polarity. Current research is directed toward new treatment options for CD that are alternatives or complementary therapeutics to a gluten-free diet. Thus, strategies to target an altered epithelial barrier therapeutically also are discussed.
Language	English
Publishing date	2017-01-14
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2819778-1
ISSN	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2016.12.006
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Article ; Online: Claudin-related intestinal diseases.

Barmeyer, Christian / Schulzke, Jörg D / Fromm, Michael

Seminars in cell & developmental biology

2015 Volume 42, Page(s) 30–38

Abstract: With up to 200 m(2) the human intestine is the organ with the largest absorptive surface of the body. It is lined by a single layer of epithelial cells that separates the host from the environment. The intestinal epithelium provides both, selective ... ...

Abstract	With up to 200 m(2) the human intestine is the organ with the largest absorptive surface of the body. It is lined by a single layer of epithelial cells that separates the host from the environment. The intestinal epithelium provides both, selective absorption of nutrients, ions, and water but also a highly effective barrier function which includes the first line of defense against environmental antigens. The paracellular part of this barrier function is provided by tight junction (TJ) proteins, especially the large family of claudins. Changes in abundance or molecular structure of claudins can generally result in three typical effects, (i) decreased absorptive passage, (ii) increased secretory passage of small solutes and water causing leak flux diarrhea and (iii) increased absorptive passage of macromolecules which may induce inflammatory processes. Several intestinal diseases are associated with such changes that can result in intestinal inflammation and symptoms like weight loss, abdominal pain or diarrhea. This review summarizes our current knowledge on barrier dysfunction and claudin dysregulation in several intestinal diseases gastroenterologists are often faced with, like inflammatory bowel disease, microscopic colitis, celiac disease, irritable bowel syndrome, gallstones and infectious diseases like HIV enteropathy, Campylobacter jejuni and Clostridium perfringens infection.
MeSH term(s)	Animals ; Biological Transport ; Claudins/metabolism ; Clostridium Infections/physiopathology ; Humans ; Intestinal Diseases/physiopathology ; Intestinal Mucosa/metabolism
Chemical Substances	Claudins
Language	English
Publishing date	2015-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1312473-0
ISSN	1096-3634 ; 1084-9521
ISSN (online)	1096-3634
ISSN	1084-9521
DOI	10.1016/j.semcdb.2015.05.006
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Article ; Online: New insights into intestinal secretion.

Schulzke, Jörg D / Siegmund, Britta / Günzel, Dorothee

Gut

2014 Volume 63, Issue 9, Page(s) 1371–1372

MeSH term(s)	Humans ; Intestinal Mucosa/secretion ; Intestinal Secretions ; Ion Channels/metabolism
Chemical Substances	Ion Channels
Language	English
Publishing date	2014-09
Publishing country	England
Document type	Journal Article
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2013-305214
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