In vitro Model of the Pathogenesis of Celiac Disease

1998 ◽  
Vol 16 (6) ◽  
pp. 341-344 ◽  
Author(s):  
Georg Oberhuber ◽  
Maria Schwarzenhofer ◽  
Harald Vogelsang
PEDIATRICS ◽  
1976 ◽  
Vol 57 (5) ◽  
pp. 715-721
Author(s):  
Aubrey J. Katz ◽  
Z. Myron Falchuk ◽  
Harry Shwachman

Two patients with cystic fibrosis (CF) who subsequently developed celiac disease (CD) are described. Since organ culture of intestinal mucosa has been used to establish an in vitro model for the study of CD, we utilized this opportunity to determine whether duodenal mucosa obtained from each of these two patients and their immediate families differed in its organ culture behavior from mucosa obtained from patients with CD alone. Additionally, as specific HL-A types are associated with CD, we used HL-A typing to determine whether the two patients with CF-CD differed genetically from patients with CD alone. One of our patients was HL-A8, the most common type associated with CD; the other was HL-A12, as are many of the non-HL-A8 celiac patients. The response in organ culture of the mucosa of these two patients was the same as the response in organ culture of the mucosa from patients with CD alone. These and other data suggest that CD occurring in patients with CF is no different than CD occurring alone.


Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 348 ◽  
Author(s):  
Federico Manai ◽  
Alberto Azzalin ◽  
Martina Morandi ◽  
Veronica Riccardi ◽  
Lisa Zanoletti ◽  
...  

Celiac disease (CD) is a chronic systemic autoimmune disorder that is triggered by the ingestion of gliadin peptides, the alcohol-soluble fraction of wheat gluten. These peptides, which play a key role in the immune response that underlies CD, spontaneously form aggregates and exert a direct toxic action on cells due to the increase in the reactive oxygen species (ROS) levels. Furthermore, peptic-tryptic digested gliadin peptides (PT-gliadin) lead to an impairment in the autophagy pathway in an in vitro model based on Caco-2 cells. Considering these premises, in this study we have analyzed different mTOR-independent inducers, reporting that the disaccharide trehalose, a mTOR-independent autophagy activator, rescued the autophagy flux in Caco-2 cells treated with digested gliadin, as well as improved cell viability. Moreover, trehalose administration to Caco-2 cells in presence of digested gliadin reduced the intracellular levels of these toxic peptides. Altogether, these results showed the beneficial effects of trehalose in a CD in vitro model as well as underlining autophagy as a molecular pathway whose modulation might be promising in counteracting PT-gliadin cytotoxicity.


2017 ◽  
Vol 14 (9) ◽  
pp. 3036-3044 ◽  
Author(s):  
Husain Attarwala ◽  
Valerie Clausen ◽  
Prasoon Chaturvedi ◽  
Mansoor M. Amiji

Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.


2011 ◽  
Vol 71 (05) ◽  
Author(s):  
M Salama ◽  
K Winkler ◽  
KF Murach ◽  
S Hofer ◽  
L Wildt ◽  
...  

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