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Article ; Online: Peculiar Ca

Sposito, Silvia / Secondo, Agnese / Romanelli, Antonio Massimiliano / Montefusco, Antonio / Nanayakkara, Merlin / Auricchio, Salvatore / Barone, Maria Vittoria / Caputo, Ivana / Paolella, Gaetana

International journal of molecular sciences

2023 Volume 24, Issue 2

Abstract: Celiac disease (CD) is an inflammatory intestinal disease caused by the ingestion of gluten-containing cereals by genetically predisposed individuals. Constitutive differences between cells from CD patients and control subjects, including levels of ... ...

Abstract	Celiac disease (CD) is an inflammatory intestinal disease caused by the ingestion of gluten-containing cereals by genetically predisposed individuals. Constitutive differences between cells from CD patients and control subjects, including levels of protein phosphorylation, alterations of vesicular trafficking, and regulation of type 2 transglutaminase (TG2), have been reported. In the present work, we investigated how skin-derived fibroblasts from CD and control subjects responded to thapsigargin, an endoplasmic reticulum ER stress inducer, in an attempt to contribute to the comprehension of molecular features of the CD cellular phenotype. We analyzed Ca
MeSH term(s)	Humans ; Celiac Disease/metabolism ; Protein Glutamine gamma Glutamyltransferase 2 ; Thapsigargin/pharmacology ; GTP-Binding Proteins/genetics ; GTP-Binding Proteins/metabolism ; Transglutaminases/genetics ; Transglutaminases/metabolism ; Autophagy ; Homeostasis
Chemical Substances	Protein Glutamine gamma Glutamyltransferase 2 (EC 2.3.2.13) ; Thapsigargin (67526-95-8) ; GTP-Binding Proteins (EC 3.6.1.-) ; Transglutaminases (EC 2.3.2.13)
Language	English
Publishing date	2023-01-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24021495
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The protective role of

Furone, Francesca / Bellomo, Claudia / Carpinelli, Martina / Nicoletti, Martina / Hewa-Munasinghege, Francesca Natasha / Mordaa, Majed / Mandile, Roberta / Barone, Maria Vittoria / Nanayakkara, Merlin

Frontiers in medicine

2023 Volume 10, Page(s) 1085578

Abstract: Celiac disease (CD) is an autoimmune enteropathy caused by an abnormal immune response to gliadin peptides in genetically predisposed individuals. For people with CD, the only available therapy thus far is the lifelong necessity for a gluten-free diet ( ... ...

Abstract	Celiac disease (CD) is an autoimmune enteropathy caused by an abnormal immune response to gliadin peptides in genetically predisposed individuals. For people with CD, the only available therapy thus far is the lifelong necessity for a gluten-free diet (GFD). Innovative therapies include probiotics and postbiotics as dietary supplements, both of which may benefit the host. Therefore, the present study aimed to investigate the possible beneficial effects of the postbiotic Lactobacillus rhamnosus GG (LGG) in preventing the effects induced by indigested gliadin peptides on the intestinal epithelium. In this study, these effects on the mTOR pathway, autophagic function, and inflammation have been evaluated. Furthermore, in this study, we stimulated the Caco-2 cells with the undigested gliadin peptide (P31-43) and with the crude gliadin peptic-tryptic peptides (PTG) and pretreated the samples with LGG postbiotics (ATCC 53103) (1 × 108). In this study, the effects induced by gliadin before and after pretreatment have also been investigated. The phosphorylation levels of mTOR, p70S6K, and p4EBP-1 were increased after treatment with PTG and P31-43, indicating that the intestinal epithelial cells responded to the gliadin peptides by activating the mTOR pathway. Moreover, in this study, an increase in the phosphorylation of NF-κβ was observed. Pretreatment with LGG postbiotic prevented both the activation of the mTOR pathway and the NF-κβ phosphorylation. In addition, P31-43 reduced LC3II staining, and the postbiotic treatment was able to prevent this reduction. Subsequently, to evaluate the inflammation in a more complex intestinal model, the intestinal organoids derived from celiac disease patient biopsies (GCD-CD) and controls (CTR) were cultured. Stimulation with peptide 31-43 in the CD intestinal organoids induced NF-κβ activation, and pretreatment with LGG postbiotic could prevent it. These data showed that the LGG postbiotic can prevent the P31-43-mediated increase in inflammation in both Caco-2 cells and in intestinal organoids derived from CD patients.
Language	English
Publishing date	2023-05-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2023.1085578
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Article ; Online: Pivotal Role of Inflammation in Celiac Disease.

Barone, Maria Vittoria / Auricchio, Renata / Nanayakkara, Merlin / Greco, Luigi / Troncone, Riccardo / Auricchio, Salvatore

International journal of molecular sciences

2022 Volume 23, Issue 13

Abstract: Celiac disease (CD) is an immune-mediated enteropathy triggered in genetically susceptible individuals by gluten-containing cereals. A central role in the pathogenesis of CD is played by the HLA-restricted gliadin-specific intestinal T cell response ... ...

Abstract	Celiac disease (CD) is an immune-mediated enteropathy triggered in genetically susceptible individuals by gluten-containing cereals. A central role in the pathogenesis of CD is played by the HLA-restricted gliadin-specific intestinal T cell response generated in a pro-inflammatory environment. The mechanisms that generate this pro-inflammatory environment in CD is now starting to be addressed. In vitro study on CD cells and organoids, shows that constant low-grade inflammation is present also in the absence of gluten. In vivo studies on a population at risk, show before the onset of the disease and before the introduction of gluten in the diet, cellular and metabolic alterations in the absence of a T cell-mediated response. Gluten exacerbates these constitutive alterations in vitro and in vivo. Inflammation, may have a main role in CD, adding this disease tout court to the big family of chronic inflammatory diseases. Nutrients can have pro-inflammatory or anti-inflammatory effects, also mediated by intestinal microbiota. The intestine function as a crossroad for the control of inflammation both locally and at distance. The aim of this review is to discuss the recent literature on the main role of inflammation in the natural history of CD, supported by cellular fragility with increased sensitivity to gluten and other pro-inflammatory agents.
MeSH term(s)	Celiac Disease/metabolism ; Gastrointestinal Microbiome ; Gliadin/metabolism ; Glutens/metabolism ; Humans ; Inflammation/pathology ; Intestinal Mucosa/metabolism
Chemical Substances	Glutens (8002-80-0) ; Gliadin (9007-90-3)
Language	English
Publishing date	2022-06-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23137177
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Article ; Online: Pivotal Role of Inflammation in Celiac Disease

Maria Vittoria Barone / Renata Auricchio / Merlin Nanayakkara / Luigi Greco / Riccardo Troncone / Salvatore Auricchio

International Journal of Molecular Sciences, Vol 23, Iss 7177, p

2022 Volume 7177

Abstract	Celiac disease (CD) is an immune-mediated enteropathy triggered in genetically susceptible individuals by gluten-containing cereals. A central role in the pathogenesis of CD is played by the HLA-restricted gliadin-specific intestinal T cell response generated in a pro-inflammatory environment. The mechanisms that generate this pro-inflammatory environment in CD is now starting to be addressed. In vitro study on CD cells and organoids, shows that constant low-grade inflammation is present also in the absence of gluten. In vivo studies on a population at risk, show before the onset of the disease and before the introduction of gluten in the diet, cellular and metabolic alterations in the absence of a T cell-mediated response. Gluten exacerbates these constitutive alterations in vitro and in vivo. Inflammation, may have a main role in CD, adding this disease tout court to the big family of chronic inflammatory diseases. Nutrients can have pro-inflammatory or anti-inflammatory effects, also mediated by intestinal microbiota. The intestine function as a crossroad for the control of inflammation both locally and at distance. The aim of this review is to discuss the recent literature on the main role of inflammation in the natural history of CD, supported by cellular fragility with increased sensitivity to gluten and other pro-inflammatory agents.
Keywords	Mediterranean and Western diet ; celiac disease ; gluten ; inflammation ; microbiota ; viral infections ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of

Conte, Mariangela / Nigro, Federica / Porpora, Monia / Bellomo, Claudia / Furone, Francesca / Budelli, Andrea Luigi / Nigro, Roberto / Barone, Maria Vittoria / Nanayakkara, Merlin

International journal of molecular sciences

2022 Volume 23, Issue 7

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 ... ...

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
MeSH term(s)	Autophagy ; Caco-2 Cells ; Celiac Disease ; Gliadin/chemistry ; Humans ; Inflammation/metabolism ; Intestinal Mucosa/metabolism ; Lactobacillus paracasei/metabolism ; Peptide Fragments/metabolism ; Peptides/pharmacology ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Peptide Fragments ; Peptides ; Gliadin (9007-90-3) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-03-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23073655
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Article ; Online: Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy

Mariangela Conte / Federica Nigro / Monia Porpora / Claudia Bellomo / Francesca Furone / Andrea Luigi Budelli / Roberto Nigro / Maria Vittoria Barone / Merlin Nanayakkara

International Journal of Molecular Sciences, Vol 23, Iss 3655, p

The Role of Lactobacillus paracasei CBA L74 Postbiotc

2022 Volume 3655

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 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Structural Perspective of Gliadin Peptides Active in Celiac Disease.

Falcigno, Lucia / Calvanese, Luisa / Conte, Mariangela / Nanayakkara, Merlin / Barone, Maria Vittoria / D'Auria, Gabriella

International journal of molecular sciences

2020 Volume 21, Issue 23

Abstract: Gluten fragments released in gut of celiac individuals activate the innate or adaptive immune systems. The molecular mechanisms associated with the adaptive response involve a series of immunodominant gluten peptides which are mainly recognized by human ... ...

Abstract	Gluten fragments released in gut of celiac individuals activate the innate or adaptive immune systems. The molecular mechanisms associated with the adaptive response involve a series of immunodominant gluten peptides which are mainly recognized by human leucocyte antigen (HLA)-DQ2.5 and HLA-DQ8. Other peptides, such as A-gliadin P31-43, are not recognized by HLA and trigger innate responses by several routes not yet well detailed. Among the gluten fragments known to be active in Celiac disease, here we focus on the properties of all gluten peptides with known tri-dimensional structure either those locked into HLA-DQ complexes whose crystals were X-ray analyzed or characterized in solution as free forms. The aim of this work was to find the structural reasons why some gluten peptides prompt the adaptive immune systems while others do not, by apparently involving just the innate immune routes. We propose that P31-43 is a non-adaptive prompter because it is not a good ligand for HLA-DQ. Even sharing a similar ability to adopt polyproline II structure with the adaptive ones, the way in which the proline residues are located along the sequence disfavors a productive P31-43-HLA-DQ binding.
MeSH term(s)	Adaptive Immunity ; Binding Sites, Antibody ; Celiac Disease/immunology ; Gliadin/chemistry ; Gliadin/immunology ; HLA-DQ Antigens/chemistry ; HLA-DQ Antigens/immunology ; Humans ; Immunity, Innate ; Molecular Docking Simulation ; Peptide Fragments/chemistry ; Peptide Fragments/immunology
Chemical Substances	HLA-DQ Antigens ; Peptide Fragments ; gliadin p31-43 ; Gliadin (9007-90-3)
Language	English
Publishing date	2020-12-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21239301
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Article ; Online: The protective role of Lactobacillus rhamnosus GG postbiotic on the alteration of autophagy and inflammation pathways induced by gliadin in intestinal models

Francesca Furone / Claudia Bellomo / Martina Carpinelli / Martina Nicoletti / Francesca Natasha Hewa-Munasinghege / Majed Mordaa / Roberta Mandile / Maria Vittoria Barone / Merlin Nanayakkara

Frontiers in Medicine, Vol

2023 Volume 10

Abstract	Celiac disease (CD) is an autoimmune enteropathy caused by an abnormal immune response to gliadin peptides in genetically predisposed individuals. For people with CD, the only available therapy thus far is the lifelong necessity for a gluten-free diet (GFD). Innovative therapies include probiotics and postbiotics as dietary supplements, both of which may benefit the host. Therefore, the present study aimed to investigate the possible beneficial effects of the postbiotic Lactobacillus rhamnosus GG (LGG) in preventing the effects induced by indigested gliadin peptides on the intestinal epithelium. In this study, these effects on the mTOR pathway, autophagic function, and inflammation have been evaluated. Furthermore, in this study, we stimulated the Caco-2 cells with the undigested gliadin peptide (P31-43) and with the crude gliadin peptic-tryptic peptides (PTG) and pretreated the samples with LGG postbiotics (ATCC 53103) (1 × 108). In this study, the effects induced by gliadin before and after pretreatment have also been investigated. The phosphorylation levels of mTOR, p70S6K, and p4EBP-1 were increased after treatment with PTG and P31-43, indicating that the intestinal epithelial cells responded to the gliadin peptides by activating the mTOR pathway. Moreover, in this study, an increase in the phosphorylation of NF-κβ was observed. Pretreatment with LGG postbiotic prevented both the activation of the mTOR pathway and the NF-κβ phosphorylation. In addition, P31-43 reduced LC3II staining, and the postbiotic treatment was able to prevent this reduction. Subsequently, to evaluate the inflammation in a more complex intestinal model, the intestinal organoids derived from celiac disease patient biopsies (GCD-CD) and controls (CTR) were cultured. Stimulation with peptide 31-43 in the CD intestinal organoids induced NF-κβ activation, and pretreatment with LGG postbiotic could prevent it. These data showed that the LGG postbiotic can prevent the P31-43-mediated increase in inflammation in both Caco-2 cells and in ...
Keywords	postbiotic ; gliadin ; organoids ; inflammation ; autophagy ; p31-43 ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2023-05-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Structural Perspective of Gliadin Peptides Active in Celiac Disease

Lucia Falcigno / Luisa Calvanese / Mariangela Conte / Merlin Nanayakkara / Maria Vittoria Barone / Gabriella D’Auria

International Journal of Molecular Sciences, Vol 21, Iss 23, p

2020 Volume 9301

Abstract	Gluten fragments released in gut of celiac individuals activate the innate or adaptive immune systems. The molecular mechanisms associated with the adaptive response involve a series of immunodominant gluten peptides which are mainly recognized by human leucocyte antigen (HLA)-DQ2.5 and HLA-DQ8. Other peptides, such as A-gliadin P31–43, are not recognized by HLA and trigger innate responses by several routes not yet well detailed. Among the gluten fragments known to be active in Celiac disease, here we focus on the properties of all gluten peptides with known tri-dimensional structure either those locked into HLA-DQ complexes whose crystals were X-ray analyzed or characterized in solution as free forms. The aim of this work was to find the structural reasons why some gluten peptides prompt the adaptive immune systems while others do not, by apparently involving just the innate immune routes. We propose that P31–43 is a non-adaptive prompter because it is not a good ligand for HLA-DQ. Even sharing a similar ability to adopt polyproline II structure with the adaptive ones, the way in which the proline residues are located along the sequence disfavors a productive P31–43-HLA-DQ binding.
Keywords	P31–43 ; NMR structure ; HLA-DQ ; innate and adaptive immune systems ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	570
Language	English
Publishing date	2020-12-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Pro-Pre and Postbiotic in Celiac Disease

Mariangela Conte / Monia Porpora / Federica Nigro / Roberto Nigro / Andrea Luigi Budelli / M. Vittoria Barone / Merlin Nanayakkara

Applied Sciences, Vol 11, Iss 8185, p

2021 Volume 8185

Abstract: Celiac Disease (CD) is an autoimmune disease characterized by inflammation of the intestinal mucosa due to an immune response to wheat gliadins. It presents in subjects with genetic susceptibility (HLA-DQ2/DQ8 positivity and non-HLA genes) and under the ... ...

Abstract	Celiac Disease (CD) is an autoimmune disease characterized by inflammation of the intestinal mucosa due to an immune response to wheat gliadins. It presents in subjects with genetic susceptibility (HLA-DQ2/DQ8 positivity and non-HLA genes) and under the influence of environmental triggers, such as viral infections and intestinal microbiota dysbiosis. The only treatment currently available in CD is a gluten-free diet for life. Despite this, the intestinal dysbiosis that is recorded in celiac subjects persists, even with adherence to dietary therapy. In this review, we have analyzed the literature over the past several decades, which have focused on the use of pro-, pre- and post-biotics in vitro and in vivo in CD. The study of probiotics and their products in CD could be interesting for observing their various effects on several different pathways, including anti-inflammatory properties.
Keywords	celiac disease ; pro- pre- and post-biotic ; inflammation ; Technology ; T ; Engineering (General). Civil engineering (General) ; TA1-2040 ; Biology (General) ; QH301-705.5 ; Physics ; QC1-999 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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