Sa244 INFLUENCE OF HELICOBACTER PYLORI ON THE MICROBIAL COMPOSITION OF HUMAN GASTRIC MUCOSA: ANALYSIS BASED ON DNA AND RNA 16S AMPLICON SEQUENCING

2021 ◽  
Vol 160 (6) ◽  
pp. S-463
Author(s):  
Elena Kupriyanova ◽  
Maria Markelova ◽  
Sayar Abdulkhakov ◽  
Tatyana Grigoryeva ◽  
Airat Safin ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tzipi Braun ◽  
Shiraz Halevi ◽  
Rotem Hadar ◽  
Gilate Efroni ◽  
Efrat Glick Saar ◽  
...  

AbstractThe coronavirus disease 2019 (COVID-19) has rapidly spread around the world, impacting the lives of many individuals. Growing evidence suggests that the nasopharyngeal and respiratory tract microbiome are influenced by various health and disease conditions, including the presence and the severity of different viral disease. To evaluate the potential interactions between Severe Acute Respiratory Syndrome Corona 2 (SARS-CoV-2) and the nasopharyngeal microbiome. Microbial composition of nasopharyngeal swab samples submitted to the clinical microbiology lab for suspected SARS-CoV-2 infections was assessed using 16S amplicon sequencing. The study included a total of 55 nasopharyngeal samples from 33 subjects, with longitudinal sampling available for 12 out of the 33 subjects. 21 of the 33 subjects had at least one positive COVID-19 PCR results as determined by the clinical microbiology lab. Inter-personal variation was the strongest factor explaining > 75% of the microbial variation, irrespective of the SARS-CoV-2 status. No significant effect of SARS-CoV-2 on the nasopharyngeal microbial community was observed using multiple analysis methods. These results indicate that unlike some other viruses, for which an effect on the microbial composition was noted, SARS-CoV-2 does not have a strong effect on the nasopharynx microbial habitants.


Gut ◽  
1990 ◽  
Vol 31 (11) ◽  
pp. 1230-1236 ◽  
Author(s):  
L L Thomsen ◽  
J B Gavin ◽  
C Tasman-Jones

2001 ◽  
Vol 96 (6) ◽  
pp. 1758-1766 ◽  
Author(s):  
Brigitte Pignatelli ◽  
Brigitte Bancel ◽  
Martin Plummer ◽  
Shinya Toyokuni ◽  
Louis-Marc Patricot ◽  
...  

1995 ◽  
Vol 108 (4) ◽  
pp. A769
Author(s):  
T. Ando ◽  
K. Kusugami ◽  
M. Sakakibara ◽  
T. Shimizu ◽  
M. Shinoda ◽  
...  

2016 ◽  
Vol 150 (4) ◽  
pp. S359
Author(s):  
Tomomitsu Tahara ◽  
Tomoyuki Shibata ◽  
Masaaki Okubo ◽  
Tomohiko Kawamura ◽  
Noriyuki Horiguchi ◽  
...  

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Satoshi Yamashita ◽  
Sohachi Nanjo ◽  
Emil Rehnberg ◽  
Naoko Iida ◽  
Hideyuki Takeshima ◽  
...  

Abstract Background Aberrant DNA methylation is induced by aging and chronic inflammation in normal tissues. The induction by inflammation is widely recognized as acceleration of age-related methylation. However, few studies addressed target genomic regions and the responsible factors in a genome-wide manner. Here, we analyzed methylation targets by aging and inflammation, taking advantage of the potent methylation induction in human gastric mucosa by Helicobacter pylori infection-triggered inflammation. Results DNA methylation microarray analysis of 482,421 CpG probes, grouped into 270,249 genomic blocks, revealed that high levels of methylation were induced in 44,461 (16.5%) genomic blocks by inflammation, even after correction of the influence of leukocyte infiltration. A total of 61.8% of the hypermethylation was acceleration of age-related methylation while 21.6% was specific to inflammation. Regions with H3K27me3 were frequently hypermethylated both by aging and inflammation. Basal methylation levels were essential for age-related hypermethylation while even regions with little basal methylation were hypermethylated by inflammation. When limited to promoter CpG islands, being a microRNA gene and high basal methylation levels strongly enhanced hypermethylation while H3K27me3 strongly enhanced inflammation-induced hypermethylation. Inflammation was capable of overriding active transcription. In young gastric mucosae, genes with high expression and frequent mutations in gastric cancers were more frequently methylated than in old ones. Conclusions Methylation by inflammation was not simple acceleration of age-related methylation. Targets of aberrant DNA methylation were different between young and old gastric mucosae, and driver genes were preferentially methylated in young gastric mucosa.


2018 ◽  
Vol 293 (44) ◽  
pp. 17248-17266 ◽  
Author(s):  
Chunsheng Jin ◽  
Angela Barone ◽  
Thomas Borén ◽  
Susann Teneberg

Helicobacter pylori has a number of well-characterized carbohydrate-binding adhesins (BabA, SabA, and LabA) that promote adhesion to the gastric mucosa. In contrast, information on the glycoconjugates present in the human stomach remains unavailable. Here, we used MS and binding of carbohydrate-recognizing ligands to characterize the glycosphingolipids of three human stomachs from individuals with different blood group phenotypes (O(Rh−)P, A(Rh+)P, and A(Rh+)p), focusing on compounds recognized by H. pylori. We observed a high degree of structural complexity, and the composition of glycosphingolipids differed among individuals with different blood groups. The type 2 chain was the dominating core chain of the complex glycosphingolipids in the human stomach, in contrast to the complex glycosphingolipids in the human small intestine, which have mainly a type 1 core. H. pylori did not bind to the O(Rh−)P stomach glycosphingolipids, whose major complex glycosphingolipids were neolactotetraosylceramide, the Lex, Lea, and H type 2 pentaosylceramides, and the Ley hexaosylceramide. Several H. pylori-binding compounds were present among the A(Rh+)P and A(Rh+)p stomach glycosphingolipids. Ligands for BabA-mediated binding of H. pylori were the Leb hexaosylceramide, the H type 1 pentaosylceramide, and the A type 1/ALeb heptaosylceramide. Additional H. pylori-binding glycosphingolipids recognized by BabA-deficient strains were lactosylceramide, lactotetraosylceramide, the x2 pentaosylceramide, and neolactohexaosylceramide. Our characterization of human gastric receptors required for H. pylori adhesion provides a basis for the development of specific compounds that inhibit the binding of this bacterium to the human gastric mucosa.


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