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Stem Cells in the Intestine: Possible Roles in Pathogenesis of Irritable Bowel Syndrome.

Ratanasirintrawoot S, Israsena N - J Neurogastroenterol Motil (2016)

Bottom Line: Interaction between intestinal stem cells and various signals from their environment is important for the control of stem cell self-renewal, regulation of number and function of specific intestinal cell types, and maintenance of the mucosal barrier.Besides their roles in stem cell regulation, these signals are also known to have potent effects on immune cells, enteric nervous system and secretory cells in the gut, and may be responsible for various aspects of pathogenesis of functional GI disorders, including visceral hypersensitivity, altered gut motility and low grade gut inflammation.In this article, we briefly summarize the components of these signaling pathways, how they can be modified by extrinsic factors and novel treatments, and provide evidenced support of their roles in the inflammation processes.

View Article: PubMed Central - PubMed

Affiliation: Stem Cell and Cell Therapy Research Unit, Chulalongkorn University, Bangkok, Thailand.

ABSTRACT
Irritable bowel syndrome is one of the most common functional gastrointestinal (GI) disorders that significantly impair quality of life in patients. Current available treatments are still not effective and the pathophysiology of this condition remains unclearly defined. Recently, research on intestinal stem cells has greatly advanced our understanding of various GI disorders. Alterations in conserved stem cell regulatory pathways such as Notch, Wnt, and bone morphogenic protein/TGF- β have been well documented in diseases such as inflammatory bowel diseases and cancer. Interaction between intestinal stem cells and various signals from their environment is important for the control of stem cell self-renewal, regulation of number and function of specific intestinal cell types, and maintenance of the mucosal barrier. Besides their roles in stem cell regulation, these signals are also known to have potent effects on immune cells, enteric nervous system and secretory cells in the gut, and may be responsible for various aspects of pathogenesis of functional GI disorders, including visceral hypersensitivity, altered gut motility and low grade gut inflammation. In this article, we briefly summarize the components of these signaling pathways, how they can be modified by extrinsic factors and novel treatments, and provide evidenced support of their roles in the inflammation processes. Furthermore, we propose how changes in these signals may contribute to the symptom development and pathogenesis of irritable bowel syndrome.

No MeSH data available.


Related in: MedlinePlus

Pathogenesis of inflammatory bowel disease (IBD). (A) Interaction between external factors such as diet and microbiota and the cells of the intestine and enteric nervous system is depicted. Panel A shows regulatory circuitry during normal repair process. (B) Panel B shows disrupted system during dys-regulated repair in IBD. Imbalanced microbiota and diet can affect stem cells and niche cells. The resulting increase in inflammatory cytokines and other signaling molecules leads to failure to maintain the stem cell pool, fate choice bias, and persistent inflammation.
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f3-jnm-22-367: Pathogenesis of inflammatory bowel disease (IBD). (A) Interaction between external factors such as diet and microbiota and the cells of the intestine and enteric nervous system is depicted. Panel A shows regulatory circuitry during normal repair process. (B) Panel B shows disrupted system during dys-regulated repair in IBD. Imbalanced microbiota and diet can affect stem cells and niche cells. The resulting increase in inflammatory cytokines and other signaling molecules leads to failure to maintain the stem cell pool, fate choice bias, and persistent inflammation.

Mentions: Taken together, Notch, Wnt and TGF-β/BMP signaling and some inflammatory cytokines play important roles in responding to external stimuli and maintaining stem cell number and function during intestinal homeostasis and repair (Fig. 3A). Imbalance of external factors such as diet and microbiota can result in dysregulation of inflammatory and non-inflammatory cytokines observed in IBD. Without proper signaling molecules, ISCs and niche cells cannot function reliably, leading to reduced number of intestinal cells, especially secretory cells, persistent activation of immune response, and hypersensitivity (Fig. 3B).


Stem Cells in the Intestine: Possible Roles in Pathogenesis of Irritable Bowel Syndrome.

Ratanasirintrawoot S, Israsena N - J Neurogastroenterol Motil (2016)

Pathogenesis of inflammatory bowel disease (IBD). (A) Interaction between external factors such as diet and microbiota and the cells of the intestine and enteric nervous system is depicted. Panel A shows regulatory circuitry during normal repair process. (B) Panel B shows disrupted system during dys-regulated repair in IBD. Imbalanced microbiota and diet can affect stem cells and niche cells. The resulting increase in inflammatory cytokines and other signaling molecules leads to failure to maintain the stem cell pool, fate choice bias, and persistent inflammation.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4930294&req=5

f3-jnm-22-367: Pathogenesis of inflammatory bowel disease (IBD). (A) Interaction between external factors such as diet and microbiota and the cells of the intestine and enteric nervous system is depicted. Panel A shows regulatory circuitry during normal repair process. (B) Panel B shows disrupted system during dys-regulated repair in IBD. Imbalanced microbiota and diet can affect stem cells and niche cells. The resulting increase in inflammatory cytokines and other signaling molecules leads to failure to maintain the stem cell pool, fate choice bias, and persistent inflammation.
Mentions: Taken together, Notch, Wnt and TGF-β/BMP signaling and some inflammatory cytokines play important roles in responding to external stimuli and maintaining stem cell number and function during intestinal homeostasis and repair (Fig. 3A). Imbalance of external factors such as diet and microbiota can result in dysregulation of inflammatory and non-inflammatory cytokines observed in IBD. Without proper signaling molecules, ISCs and niche cells cannot function reliably, leading to reduced number of intestinal cells, especially secretory cells, persistent activation of immune response, and hypersensitivity (Fig. 3B).

Bottom Line: Interaction between intestinal stem cells and various signals from their environment is important for the control of stem cell self-renewal, regulation of number and function of specific intestinal cell types, and maintenance of the mucosal barrier.Besides their roles in stem cell regulation, these signals are also known to have potent effects on immune cells, enteric nervous system and secretory cells in the gut, and may be responsible for various aspects of pathogenesis of functional GI disorders, including visceral hypersensitivity, altered gut motility and low grade gut inflammation.In this article, we briefly summarize the components of these signaling pathways, how they can be modified by extrinsic factors and novel treatments, and provide evidenced support of their roles in the inflammation processes.

View Article: PubMed Central - PubMed

Affiliation: Stem Cell and Cell Therapy Research Unit, Chulalongkorn University, Bangkok, Thailand.

ABSTRACT
Irritable bowel syndrome is one of the most common functional gastrointestinal (GI) disorders that significantly impair quality of life in patients. Current available treatments are still not effective and the pathophysiology of this condition remains unclearly defined. Recently, research on intestinal stem cells has greatly advanced our understanding of various GI disorders. Alterations in conserved stem cell regulatory pathways such as Notch, Wnt, and bone morphogenic protein/TGF- β have been well documented in diseases such as inflammatory bowel diseases and cancer. Interaction between intestinal stem cells and various signals from their environment is important for the control of stem cell self-renewal, regulation of number and function of specific intestinal cell types, and maintenance of the mucosal barrier. Besides their roles in stem cell regulation, these signals are also known to have potent effects on immune cells, enteric nervous system and secretory cells in the gut, and may be responsible for various aspects of pathogenesis of functional GI disorders, including visceral hypersensitivity, altered gut motility and low grade gut inflammation. In this article, we briefly summarize the components of these signaling pathways, how they can be modified by extrinsic factors and novel treatments, and provide evidenced support of their roles in the inflammation processes. Furthermore, we propose how changes in these signals may contribute to the symptom development and pathogenesis of irritable bowel syndrome.

No MeSH data available.


Related in: MedlinePlus