Gotowa bibliografia na temat „Immunologie de l’intestin”
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Artykuły w czasopismach na temat "Immunologie de l’intestin"
Bouchikhi, I., H. Kaddouri, L. Amier, O. Kheroua i J. Saidi. "Effet de la dose sensibilisante de l’ovalbumine sur l’intestin de souris Balb/c". Revue Française d'Allergologie 54, nr 3 (kwiecień 2014): 251. http://dx.doi.org/10.1016/j.reval.2014.02.086.
Pełny tekst źródłaVillafana, L., C. Dupont i F. Ruemmele. "Allergies alimentaires et maladies inflammatoires de l’intestin des enfants et adolescents : y a-t-il une relation ?" Revue Française d'Allergologie 53, nr 3 (kwiecień 2013): 338. http://dx.doi.org/10.1016/j.reval.2013.02.021.
Pełny tekst źródłaEl Mecherfi, K. E., Y. Bouferkas, D. Saidi i O. Kheroua. "Impact des gliadines sur les paramètres électrophysiologiques de l’intestin étudié chez le modèle animal d’allergie au blé". Revue Française d'Allergologie 56, nr 3 (kwiecień 2016): 330. http://dx.doi.org/10.1016/j.reval.2016.02.199.
Pełny tekst źródłaAyad, N., B. Hellal i M. Maatoug. "Sensibilisation parentérale du lapin aux protéines du lait de vache : effets sur les paramètres électrophysiologiques de l’intestin". Revue Française d'Allergologie et d'Immunologie Clinique 48, nr 1 (styczeń 2008): 9–13. http://dx.doi.org/10.1016/j.allerg.2007.08.011.
Pełny tekst źródłaAddou, S., N. Youcef, M. Belmaloufi i O. Kheroua. "Identification et caractérisation des bactéries pathogènes dans l’intestin des souris Balb/C immunisées à la β-lg et l’α-lac bovine et nourris au lait de chamelle". Revue Française d'Allergologie 61, nr 4 (maj 2021): 234. http://dx.doi.org/10.1016/j.reval.2021.03.016.
Pełny tekst źródłaRozprawy doktorskie na temat "Immunologie de l’intestin"
Nawrot, Margaux. "Rôle du récepteur nucléaire Farnesoid X Receptor intestinal dans la fonction immune de l’intestin dans le contexte physiopathologique de la stéatohépatite non alcoolique". Thesis, Université de Lille (2018-2021), 2021. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2021/2021LILUS053.pdf.
Pełny tekst źródłaEnergy homeostasis is the result of a dialogue between metabolic organs, especially gut and liver. The intestine is an interface between the organism and the external environment. Its role as a barrier is possible thanks to a complex immune system and intercellular junctions. In metabolic diseases such as type 2 diabetes and non-alcoholic steatohepatitis (NASH), there is an increase in systemic low-grade inflammation, particularly in intestine, and an increase in intestinal permeability. The nuclear bile acid receptor, Farnesoid X Receptor (FXR), is expressed in metabolic organs. FXR Knock-Out (KO) mice fed a standard diet show increased intestinal permeability compared to their littermate controls, although they are protected against high-fat diet-induced obesity and insulin resistance. The role of FXR in the intestine is reported in a more contradictory way in the literature because according to the studies its inactivation in the epithelium decreases the synthesis of ceramides which would then contribute to protect the liver from steatosis, and its activation induces the browning of adipose tissue, reducing obesity and insulin resistance. In this context, we wanted to understand whether gut immune functions are under the control of intestinal FXR in a nutritional context inducing NASH.At the beginning of my thesis, I participated in the establishment in the laboratory of the breeding of mice deficient in FXR only in the intestine (intFXR KO) by a cre-lox system. The model was validated and the metabolic status of the mice on a standard diet was checked. Although intFXR KO mice appeared to have similar hepatic histological characteristics to control mice, the expression of genes related to innate immunity is perturbed suggesting that intestinal FXR deficiency may alter the hepatic and global inflammatory state. By immunophenotyping, we showed that cytotoxic lymphocytes (CD8+ TL) are increased in the intestine of intFXR KO mice. This change may be due to an increase in circulating CD8+ TL targeting the intestine. This disruption of intestinal immunity may be due to a decrease in the expression of tight junction proteins that would facilitate the passage of microbial products. The study of the gut microbiota of intFXR KO mice shows an increase in a bacterial population reported to be involved in colitis.Our next objective was to study the consequences of intestinal FXR deficiency in a nutritional context inducing NASH in 24 weeks. We found that were well protected against hepatic steatosis, gut transcriptomic analysis suggesting a modulation of intestinal lipid metabolism. However, intFXR KO mice are not protected against the development of NASH and FXR deficiency in the gut would even amplify the expression of inflammation-related genes in the liver compared to control mice. In intFXR KO mice, we observed an increase in CD8+ TLs, an increase in intestinal permeability markers and intestinal bacterial populations described in inflammatory bowel disease.Thus, while protecting against weight gain and hepatic steatosis, intestinal FXR deficiency appears to amplify hepatic inflammation under standard and also NASH nutritional conditions. Modulation of intestinal immunity by FXR agonists therefore appears to be an interesting approach to modulate the gut-liver dialogue in the treatment of NASH