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Article

Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of Lactobacillus paracasei CBA L74 Postbiotc

by
Mariangela Conte
1,
Federica Nigro
2,
Monia Porpora
1,
Claudia Bellomo
1,
Francesca Furone
1,
Andrea Luigi Budelli
3,
Roberto Nigro
3,
Maria Vittoria Barone
1,* and
Merlin Nanayakkara
1
1
ELFID (European Laboratory for the Investigation of Food Induced Diseases), Department of Translational Medical Science, Section of Paediatrics, University Federico II, Via S. Pansini 5, 80131 Naples, Italy
2
I.T.P. Innovation and Technology Provider s.r.l., Via Bisignano a Chiaia 68, 80121 Naples, Italy
3
DICMAPI, University of Naples Federico II, 80125 Naples, Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2022, 23(7), 3655; https://doi.org/10.3390/ijms23073655
Submission received: 10 February 2022 / Revised: 18 March 2022 / Accepted: 24 March 2022 / Published: 26 March 2022
(This article belongs to the Special Issue Pro-inflammatory Nutrients: Focus on Gliadin and Celiac Disease 2.0)
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Abstract

Celiac disease (CD) is an autoimmune disease characterized by an altered immune response stimulated by gliadin peptides that are not digested and cause damage to the intestinal mucosa. The aim of this study was to investigate whether the postbiotic Lactobacillus paracasei (LP) could prevent the action of gliadin peptides on mTOR, autophagy, and the inflammatory response. Most of the experiments performed were conducted on intestinal epithelial cells Caco-2 treated with a peptic-tryptic digest of gliadin (PTG) and P31-43. Furthermore, we pretreated the Caco-2 with the postbiotic LP before treatment with the previously described stimuli. In both cases, we evaluated the levels of pmTOR, p70S6k, and p4EBP-1 for the mTOR pathway, pNFkβ, and pERK for inflammation and LC 3 and p62 for autophagy. For autophagy, we also used immunofluorescence analysis. Using intestinal organoids derivate from celiac (CD) patients, we analyzed the effect of gliadin after postbiotic pretreatment with LP on inflammation marker NFkβ. Through these experiments, we showed that gliadin peptides are able to induce the increase of the inflammatory response in a more complex model of intestinal epithelial cells. LP postbiotic was able to induce autophagy in Caco-2 cells and prevent gliadin effects. In conclusion, postbiotic pretreatment with LP could be considered for in vivo clinical trials.
Keywords: celiac disease (CD); gliadin peptide P31-43; mTOR/NFkβ activation; Lactobacillus paracasei CBA L74 postbiotc celiac disease (CD); gliadin peptide P31-43; mTOR/NFkβ activation; Lactobacillus paracasei CBA L74 postbiotc

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MDPI and ACS Style

Conte, M.; Nigro, F.; Porpora, M.; Bellomo, C.; Furone, F.; Budelli, A.L.; Nigro, R.; Barone, M.V.; Nanayakkara, M. Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of Lactobacillus paracasei CBA L74 Postbiotc. Int. J. Mol. Sci. 2022, 23, 3655. https://doi.org/10.3390/ijms23073655

AMA Style

Conte M, Nigro F, Porpora M, Bellomo C, Furone F, Budelli AL, Nigro R, Barone MV, Nanayakkara M. Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of Lactobacillus paracasei CBA L74 Postbiotc. International Journal of Molecular Sciences. 2022; 23(7):3655. https://doi.org/10.3390/ijms23073655

Chicago/Turabian Style

Conte, Mariangela, Federica Nigro, Monia Porpora, Claudia Bellomo, Francesca Furone, Andrea Luigi Budelli, Roberto Nigro, Maria Vittoria Barone, and Merlin Nanayakkara. 2022. "Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of Lactobacillus paracasei CBA L74 Postbiotc" International Journal of Molecular Sciences 23, no. 7: 3655. https://doi.org/10.3390/ijms23073655

APA Style

Conte, M., Nigro, F., Porpora, M., Bellomo, C., Furone, F., Budelli, A. L., Nigro, R., Barone, M. V., & Nanayakkara, M. (2022). Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of Lactobacillus paracasei CBA L74 Postbiotc. International Journal of Molecular Sciences, 23(7), 3655. https://doi.org/10.3390/ijms23073655

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