Lipopolysaccharides From Non-Helicobacter pylori Gastric Bacteria Potently Stimulate Interleukin-8 Production in Gastric Epithelial Cells.
Cell Line
Epithelial Cells
/ drug effects
Gastric Mucosa
/ metabolism
Helicobacter Infections
/ metabolism
Helicobacter pylori
/ physiology
Humans
Interleukin-8
/ metabolism
Lipopolysaccharide Receptors
/ metabolism
Lipopolysaccharides
/ pharmacology
Neisseria
/ physiology
Toll-Like Receptor 2
/ metabolism
Toll-Like Receptor 4
/ metabolism
Journal
Clinical and translational gastroenterology
ISSN: 2155-384X
Titre abrégé: Clin Transl Gastroenterol
Pays: United States
ID NLM: 101532142
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
pubmed:
27
3
2019
medline:
22
5
2020
entrez:
27
3
2019
Statut:
ppublish
Résumé
Gastric acid secretion is compromised in chronic Helicobacter pylori (H. pylori) infection allowing overgrowth of non-H. pylori gastric bacteria (NHGB) in the stomach. NHGB were isolated from gastric mucosa in selective media and further characterized with biochemical methods and 16S rRNA gene sequencing. Human gastric tissues were studied with indirect immunofluorescence with antibodies against H. pylori and Neisseria subflava (N. subflava). Gastric epithelial cell lines were cocultured with bacteria or incubated with lipopolysaccharides isolated from NHGB, and interleukin-8 released in the media was measured by enzyme-linked immunosorbent assay. Expression of Toll-like receptor (TLR)2, TLR4, it's coreceptor myeloid differentiation factor 2 (MD2), and CD14 in gastric cells was investigated by immunofluorescence microscopy and reverse transcriptase-polymerase chain reaction. Haemophilus species, Neisseria species, Fusobacterium species, and Veillonella species were predominant Gram-negative bacteria coinfected with H. pylori. Lipopolysaccharides from N. subflava potently stimulated interleukin-8 secretion in MKN45 cells which was cancelled by preincubation with polymyxin B. TLR2, TLR4, CD14, and myeloid differentiation factor 2 were expressed in MKN45 cells, though their levels of expression were low. N. subflava adhered to MKN45 cells in vitro and colocalized with H. pylori in the human gastric mucosa. Our data suggest that N. subflava colonized in the gastric mucosa contribute to gastric inflammation during chronic H. pylori gastritis. NHGB may perpetuate gastric inflammation and accelerate neoplastic progression in the hypochlorhydric stomach.
Sections du résumé
BACKGROUND
Gastric acid secretion is compromised in chronic Helicobacter pylori (H. pylori) infection allowing overgrowth of non-H. pylori gastric bacteria (NHGB) in the stomach.
METHODS
NHGB were isolated from gastric mucosa in selective media and further characterized with biochemical methods and 16S rRNA gene sequencing. Human gastric tissues were studied with indirect immunofluorescence with antibodies against H. pylori and Neisseria subflava (N. subflava). Gastric epithelial cell lines were cocultured with bacteria or incubated with lipopolysaccharides isolated from NHGB, and interleukin-8 released in the media was measured by enzyme-linked immunosorbent assay. Expression of Toll-like receptor (TLR)2, TLR4, it's coreceptor myeloid differentiation factor 2 (MD2), and CD14 in gastric cells was investigated by immunofluorescence microscopy and reverse transcriptase-polymerase chain reaction.
RESULTS
Haemophilus species, Neisseria species, Fusobacterium species, and Veillonella species were predominant Gram-negative bacteria coinfected with H. pylori. Lipopolysaccharides from N. subflava potently stimulated interleukin-8 secretion in MKN45 cells which was cancelled by preincubation with polymyxin B. TLR2, TLR4, CD14, and myeloid differentiation factor 2 were expressed in MKN45 cells, though their levels of expression were low. N. subflava adhered to MKN45 cells in vitro and colocalized with H. pylori in the human gastric mucosa.
CONCLUSIONS
Our data suggest that N. subflava colonized in the gastric mucosa contribute to gastric inflammation during chronic H. pylori gastritis.
TRANSLATIONAL IMPACT
NHGB may perpetuate gastric inflammation and accelerate neoplastic progression in the hypochlorhydric stomach.
Identifiants
pubmed: 30913125
doi: 10.14309/ctg.0000000000000024
pmc: PMC6445647
doi:
Substances chimiques
Interleukin-8
0
Lipopolysaccharide Receptors
0
Lipopolysaccharides
0
TLR2 protein, human
0
Toll-Like Receptor 2
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
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