scholarly journals Accumulation of abasic sites induces genomic instability in normal human gastric epithelial cells during Helicobacter pylori infection

Oncogenesis ◽  
2014 ◽  
Vol 3 (11) ◽  
pp. e128-e128 ◽  
Author(s):  
D Kidane ◽  
D L Murphy ◽  
J B Sweasy
2018 ◽  
Vol 9 (5) ◽  
pp. 829-841 ◽  
Author(s):  
V. Garcia-Castillo ◽  
H. Zelaya ◽  
A. Ilabaca ◽  
M. Espinoza-Monje ◽  
R. Komatsu ◽  
...  

Helicobacter pylori infection is associated with important gastric pathologies. An aggressive proinflammatory immune response is generated in the gastric tissue infected with H. pylori, resulting in gastritis and a series of morphological changes that increase the susceptibility to cancer development. Probiotics could present an alternative solution to prevent or decrease H. pylori infection. Among them, the use of immunomodulatory lactic acid bacteria represents a promising option to reduce the severity of chronic inflammatory-mediated tissue damage and to improve protective immunity against H. pylori. We previously isolated Lactobacillus fermentum UCO-979C from human gastric tissue and demonstrated its capacity to reduce adhesion of H. pylori to human gastric epithelial cells (AGS cells). In this work, the ability of L. fermentum UCO-979C to modulate immune response in AGS cells and PMA phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 (human monocytic leukaemia) macrophages in response to H. pylori infection was evaluated. We demonstrated that the UCO-979C strain is able to differentially modulate the cytokine response of gastric epithelial cells and macrophages after H. pylori infection. Of note, L. fermentum UCO-979C was able to significantly reduce the production of inflammatory cytokines and chemokines in AGS and THP-1 cells as well as increase the levels of immunoregulatory cytokines, indicating a remarkable anti-inflammatory effect. These findings strongly support the probiotic potential of L. fermentum UCO-979C and provide evidence of its beneficial effects against the inflammatory damage induced by H. pylori infection. Although our findings should be proven in appropriate experiments in vivo, in both H. pylori infection animal models and human trials, the results of the present work provide a scientific rationale for the use of L. fermentum UCO-979C to prevent or reduce H. pylori-induced gastric inflammation in humans.


2018 ◽  
Vol 116 ◽  
pp. 120-123 ◽  
Author(s):  
Seiran Zandi ◽  
Manouchehr A. Hedayati ◽  
Ebrahim Mohammadi ◽  
Farshad Sheikhesmaeili

2003 ◽  
Vol 124 (4) ◽  
pp. A589
Author(s):  
Takeshi Azuma ◽  
Shiho Yamazaki ◽  
Akiyo Yamakawa ◽  
Masahiro Ohtani ◽  
Yoshiyuki Ito ◽  
...  

2003 ◽  
Vol 124 (4) ◽  
pp. A43 ◽  
Author(s):  
Jerome Viala ◽  
Catherine Chaput ◽  
Ivo G. Boneca ◽  
Stephen E. Girardin ◽  
Anthony P. Moran ◽  
...  

Helicobacter ◽  
2002 ◽  
Vol 7 (5) ◽  
pp. 271-280 ◽  
Author(s):  
S. M. Everett ◽  
K. L. M. White ◽  
I. M. Drake ◽  
C. J. Schorah ◽  
R. J. Calvert ◽  
...  

PLoS ONE ◽  
2019 ◽  
Vol 14 (8) ◽  
pp. e0220636 ◽  
Author(s):  
Weronika Gonciarz ◽  
Agnieszka Krupa ◽  
Krzysztof Hinc ◽  
Michał Obuchowski ◽  
Anthony P Moran ◽  
...  

2011 ◽  
Vol 135 (6) ◽  
pp. 759-765
Author(s):  
So-Hyun Shin ◽  
Seog-Yun Park ◽  
Jae-Sung Ko ◽  
Nayoung Kim ◽  
Gyeong Hoon Kang

Abstract Context.—Helicobacter pylori infection is primarily acquired during childhood and persists throughout life in the absence of eradication with antibiotics. Helicobacter pylori infection induces methylation in the promoter CpG island loci in gastric epithelial cells. Thus, aberrant CpG island hypermethylation in gastric epithelial cells likely occurs early in life, although there are no existing data supporting this notion. Objectives.—To identify whether aberrant CpG island hypermethylation occurs in pediatric stomach mucosa in association with H pylori infection and to compare methylation profiles of samples from pediatric and adult stomach tissues. Design.—We analyzed pediatric (n  =  47) and adult (n  =  38) gastric mucosa samples for their methylation status in 12 promoter CpG island loci using the MethyLight assay and compared the number of methylated genes and the methylation levels in individual genes between H pylori–positive and H pylori–negative sample results and between pediatric and adult samples. Results.—The average number of methylated genes was significantly higher in H pylori–infected pediatric samples than in H pylori–negative pediatric samples (3.4 versus 0.3, P < .001) and in H pylori–infected adult samples than in H pylori–negative adult samples (7.6 versus 0.9, P < .001). Seven genes showed significantly higher methylation levels in H pylori–infected pediatric samples than in H pylori–negative pediatric samples (all values were P < .05). Conclusions.—These results indicate that CpG island hypermethylation occurs in pediatric gastric mucosa in association with H pylori infection and that the genes affected by H pylori–associated hypermethylation were similar in pediatric and adult samples.


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