scholarly journals Creatine Transporter, Reduced in Colon Tissues From Patients With Inflammatory Bowel Diseases, Regulates Energy Balance in Intestinal Epithelial Cells, Epithelial Integrity, and Barrier Function

2020 ◽  
Vol 159 (3) ◽  
pp. 984-998.e1 ◽  
Author(s):  
Caroline H.T. Hall ◽  
J. Scott Lee ◽  
Emily M. Murphy ◽  
Mark E. Gerich ◽  
Rachael Dran ◽  
...  
Keyword(s):  
Energy Balance ◽  
Epithelial Cells ◽  
Inflammatory Bowel Diseases ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Creatine Transporter ◽  
Epithelial Integrity ◽  
Bowel Diseases ◽  
Inflammatory Bowel

scholarly journals Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Wakana Ohashi ◽  
Toshiyuki Fukada
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Bowel Diseases ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Gastrointestinal Diseases ◽  
Zinc Transporters ◽  
Intestinal Epithelial ◽  
Self Renewal ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Intestinal epithelial cells cover the surface of the intestinal tract. The cells are important for preserving the integrity of the mucosal barriers to protect the host from luminal antigens and pathogens. The mucosal barriers are maintained by the continuous and rapid self-renewal of intestinal epithelial cells. Defects in the self-renewal of these cells are associated with gastrointestinal diseases, including inflammatory bowel diseases and diarrhea. Zinc is an essential trace element for living organisms, and zinc deficiency is closely linked to the impaired mucosal integrity. Recent evidence has shown that zinc transporters contribute to the barrier function of intestinal epithelial cells. In this review, we describe the recent advances in understanding the role of zinc and zinc transporters in the barrier function and homeostasis of intestinal epithelial cells.

Proteomic response of inflammatory stimulated intestinal epithelial cells to in vitro digested plums and cabbages rich in carotenoids and polyphenols

2016 ◽  
Vol 7 (10) ◽  
pp. 4388-4399 ◽  
Author(s):  
Anouk Kaulmann ◽  
Sébastien Planchon ◽  
Jenny Renaut ◽  
Yves-Jacques Schneider ◽  
Lucien Hoffmann ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Bowel Diseases ◽  
Intestinal Epithelial Cells ◽  
Intestinal Cells ◽  
Intestinal Epithelial ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Proteomic Response

Proteomic response of intestinal cells as a model of inflammatory bowel diseases to digested plum and cabbage rich in polyphenols and carotenoids.

Signaling pathway via TNF-α/NF-κB in intestinal epithelial cells may be directly involved in colitis-associated carcinogenesis

2009 ◽  
Vol 296 (4) ◽  
pp. G850-G859 ◽  
Author(s):  
Michio Onizawa ◽  
Takashi Nagaishi ◽  
Takanori Kanai ◽  
Ken-ichi Nagano ◽  
Shigeru Oshima ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Maintenance Therapy ◽  
Intestinal Epithelial Cells ◽  
Immunoblot Analysis ◽  
Intestinal Epithelial ◽  
Tnf Receptor ◽  
Tnf Α ◽  
Sequential Administration ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Treatment with anti-TNF-α MAb has been accepted as a successful maintenance therapy for patients with inflammatory bowel diseases (IBD). Moreover, it has been recently reported that blockade of TNF receptor (TNFR) 1 signaling in infiltrating hematopoietic cells may prevent the development of colitis-associated cancer (CAC). However, it remains unclear whether the TNF-α signaling in epithelial cells is involved in the development of CAC. To investigate this, we studied the effects of anti-TNF-α MAb in an animal model of CAC by administration of azoxymethane (AOM) followed by sequential dextran sodium sulfate (DSS) ingestion. We observed that the NF-κB pathway is activated in colonic epithelia from DSS-administered mice in association with upregulation of TNFR2 rather than TNFR1. Immunoblot analysis also revealed that the TNFR2 upregulation accompanied by the NF-κB activation is further complicated in CAC tissues induced in AOM/DSS-administered mice compared with the nontumor area. Such NF-κB activity in the epithelial cells is significantly suppressed by the treatment of MP6-XT22, an anti-TNF-α MAb. Despite inability to reduce the severity of colitis, sequential administration of MP6-XT22 reduced the numbers and size of tumors in association with the NF-κB inactivation. Taken together, present studies suggest that the TNFR2 signaling in intestinal epithelial cells may be directly involved in the development of CAC with persistent colitis and imply that the maintenance therapy with anti-TNF-α MAb may prevent the development of CAC in patients with long-standing IBD.

scholarly journals Innate Lymphoid Cells as Regulators of Epithelial Integrity: Therapeutic Implications for Inflammatory Bowel Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Anja Schulz-Kuhnt ◽  
Markus F. Neurath ◽  
Stefan Wirtz ◽  
Imke Atreya
Keyword(s):  
Epithelial Cell ◽  
Immune Cells ◽  
Inflammatory Bowel Diseases ◽  
Innate Lymphoid Cells ◽  
Experimental Models ◽  
Lymphoid Cells ◽  
Intestinal Epithelial ◽  
Epithelial Integrity ◽  
Bowel Diseases ◽  
Inflammatory Bowel

The occurrence of epithelial defects in the gut relevantly contributes to the pathogenesis of inflammatory bowel diseases (IBD), whereby the impairment of intestinal epithelial barrier integrity seems to represent a primary trigger as well as a disease amplifying consequence of the chronic inflammatory process. Besides epithelial cell intrinsic factors, accumulated and overwhelmingly activated immune cells and their secretome have been identified as critical modulators of the pathologically altered intestinal epithelial cell (IEC) function in IBD. In this context, over the last 10 years increasing levels of attention have been paid to the group of innate lymphoid cells (ILCs). This is in particular due to a preferential location of these rather newly described innate immune cells in close proximity to mucosal barriers, their profound capacity to secrete effector cytokines and their numerical and functional alteration under chronic inflammatory conditions. Aiming on a comprehensive and updated summary of our current understanding of the bidirectional mucosal crosstalk between ILCs and IECs, this review article will in particular focus on the potential capacity of gut infiltrating type-1, type-2, and type-3 helper ILCs (ILC1s, ILC2s, and ILC3s, respectively) to impact on the survival, differentiation, and barrier function of IECs. Based on data acquired in IBD patients or in experimental models of colitis, we will discuss whether the different ILC subgroups could serve as potential therapeutic targets for maintenance of epithelial integrity and/or mucosal healing in IBD.

scholarly journals Toll-like receptors 2 and 4 modulate intestinal IL-10 differently in ileum and colon

2017 ◽  
Vol 6 (3) ◽  
pp. 446-453 ◽  
Author(s):  
Eva Latorre ◽  
Elena Layunta ◽  
Laura Grasa ◽  
Julián Pardo ◽  
Santiago García ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cell Model ◽  
Immune Recognition ◽  
Intestinal Epithelial ◽  
Intestinal Homeostasis ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Gram Negative Organisms ◽  
Tlr4 Activation

Background Inflammatory bowel diseases are consequence of an intestinal homeostasis breakdown in which innate immune dysregulation is implicated. Toll-like receptor (TLR)2 and TLR4 are immune recognition receptors expressed in the intestinal epithelium, the first physical-physiological barrier for microorganisms, to inform the host of the presence of Gram-positive and Gram-negative organisms. Interleukin (IL)-10 is an essential anti-inflammatory cytokine that contributes to maintenance of intestinal homeostasis. Aim Our main aim was to investigate intestinal IL-10 synthesis and release, and whether TLR2 and TLR4 are determinants of IL-10 expression in the intestinal tract. Methods We used Caco-2 cell line as an enterocyte-like cell model, and also ileum and colon from mice deficient in TLR2, TLR4 or TLR2/4 to test the involvement of TLR signaling. Results Intestinal epithelial cells are able to synthesize and release IL-10 and their expression is increased after TLR2 or TLR4 activation. IL-10 regulation seems to be tissue specific, with IL-10 expression in the ileum regulated by a compensation between TLR2 and TLR4 expression, whereas in the colon, TLR2 and TLR4 affect IL-10 expression independently. Conclusions Intestinal epithelial cells could release IL-10 in response to TLR activation, playing an intestinal tissue-dependent and critical intestinal immune role.

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