Celiac disease-associated Neisseria flavescens decreases mitochondrial respiration in CaCo-2 epithelial cells: Impact of Lactobacillus paracasei CBA L74 on bacterial-induced cellular imbalance.
Adenosine Triphosphate
/ agonists
Autophagosomes
/ drug effects
Autophagy
/ drug effects
Caco-2 Cells
Celiac Disease
/ metabolism
Culture Media, Conditioned
/ pharmacology
Dysbiosis
/ metabolism
Gene Expression
Gliadin
/ antagonists & inhibitors
Host-Pathogen Interactions
/ drug effects
Humans
Lacticaseibacillus paracasei
/ chemistry
Lysosomal-Associated Membrane Protein 2
/ genetics
Microtubule-Associated Proteins
/ genetics
Mitochondria
/ drug effects
Neisseria
/ drug effects
Oxidative Phosphorylation
/ drug effects
Peptide Fragments
/ antagonists & inhibitors
Probiotics
/ pharmacology
Thiobarbituric Acid Reactive Substances
/ metabolism
Transport Vesicles
/ drug effects
Vesicular Transport Proteins
/ genetics
CaCo-2 cells
L. paracasei CBA L74 probiotic
Neisseria flavescens
P31-43 gliadin peptide
celiac disease
Journal
Cellular microbiology
ISSN: 1462-5822
Titre abrégé: Cell Microbiol
Pays: India
ID NLM: 100883691
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
17
11
2018
revised:
10
04
2019
accepted:
22
04
2019
pubmed:
2
5
2019
medline:
29
8
2020
entrez:
2
5
2019
Statut:
ppublish
Résumé
We previously identified a Neisseria flavescens strain in the duodenum of celiac disease (CD) patients that induced immune inflammation in ex vivo duodenal mucosal explants and in CaCo-2 cells. We also found that vesicular trafficking was delayed after the CD-immunogenic P31-43 gliadin peptide-entered CaCo-2 cells and that Lactobacillus paracasei CBA L74 (L. paracasei-CBA) supernatant reduced peptide entry. In this study, we evaluated if metabolism and trafficking was altered in CD-N. flavescens-infected CaCo-2 cells and if any alteration could be mitigated by pretreating cells with L. paracasei-CBA supernatant, despite the presence of P31-43. We measured CaCo-2 bioenergetics by an extracellular flux analyser, N. flavescens and P31-43 intracellular trafficking by immunofluorescence, cellular stress by TBARS assay, and ATP by bioluminescence. We found that CD-N. flavescens colocalised more than control N. flavescens with early endocytic vesicles and more escaped autophagy thereby surviving longer in infected cells. P31-43 increased colocalisation of N. flavescens with early vesicles. Mitochondrial respiration was lower (P < .05) in CD-N. flavescens-infected cells versus not-treated CaCo-2 cells, whereas pretreatment with L. paracasei-CBA reduced CD-N. flavescens viability and improved cell bioenergetics and trafficking. In conclusion, CD-N. flavescens induces metabolic imbalance in CaCo-2 cells, and the L. paracasei-CBA probiotic could be used to correct CD-associated dysbiosis.
Identifiants
pubmed: 31042331
doi: 10.1111/cmi.13035
pmc: PMC6618323
doi:
Substances chimiques
Culture Media, Conditioned
0
LAMP2 protein, human
0
Lysosomal-Associated Membrane Protein 2
0
MAP1LC3A protein, human
0
Microtubule-Associated Proteins
0
Peptide Fragments
0
Thiobarbituric Acid Reactive Substances
0
Vesicular Transport Proteins
0
early endosome antigen 1
0
gliadin peptide (31-43)
0
Adenosine Triphosphate
8L70Q75FXE
Gliadin
9007-90-3
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13035Informations de copyright
© 2019 The Authors Cellular Microbiology Published by John Wiley & Sons Ltd.
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