Dysbiosis of the microbiome in gastric carcinogenesis

• Published in: Scientific reports Vol. 7; no. 1; pp. 15957 - 9
• Main Authors: Castaño-Rodríguez, Natalia, Goh, Khean-Lee, Fock, Kwong Ming, Mitchell, Hazel M., Kaakoush, Nadeem O.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 21-11-2017; Nature Publishing Group; Nature Portfolio
• Subjects: 45/23; 45/90; 45/91; 631/326/2565/2134; 692/699/1503/1828/1829; Acid production; Bacteria; Carcinogenesis; Dysbacteriosis; Dyspepsia; Gastric cancer; Humanities and Social Sciences; Inflammation; Lactic acid; Metabolism; Microbiota; multidisciplinary; Phylogeny; rRNA 16S; Science; Science (multidisciplinary)
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-017-16289-2

The gastric microbiome has been proposed as an etiological factor in gastric carcinogenesis. We compared the gastric microbiota in subjects presenting with gastric cancer (GC, n = 12) and controls (functional dyspepsia (FD), n = 20) from a high GC risk population in Singapore and Malaysia. cDNA from 16S rRNA transcripts were amplified (515F-806R) and sequenced using Illumina MiSeq 2 × 250 bp chemistry. Increased richness and phylogenetic diversity but not Shannon’s diversity was found in GC as compared to controls. nMDS clustered GC and FD subjects separately, with PERMANOVA confirming a significant difference between the groups.
H. pylori
serological status had a significant impact on gastric microbiome α-diversity and composition. Several bacterial taxa were enriched in GC, including
Lactococcus
,
Veilonella
, and
Fusobacteriaceae
(
Fusobacterium
and
Leptotrichia
). Prediction of bacterial metabolic contribution indicated that serological status had a significant impact on metabolic function, while carbohydrate digestion and pathways were enriched in GC. Our findings highlight three mechanisms of interest in GC, including enrichment of pro-inflammatory oral bacterial species, increased abundance of lactic acid producing bacteria, and enrichment of short chain fatty acid production pathways.