Molecular characterization of the stomach microbiota in patients with gastric cancer and in controls.
Persistent infection of the gastric mucosa by Helicobacter pylori can initiate an inflammatory cascade that progresses into atrophic gastritis, a condition associated with reduced capacity for secretion of gastric acid and an increased risk of developing gastric cancer. The role of H. pylori as an initiator of inflammation is evident but the mechanism for development into gastric cancer has not yet been proven. A reduced capacity for gastric acid secretion allows survival and proliferation of other microbes that normally are killed by the acidic environment. It has been postulated that some of these species may be involved in the development of gastric cancer; however, their identities are poorly defined. In this study, the gastric microbiota from ten patients with gastric cancer was characterized and compared with that from five dyspeptic controls using the molecular profiling approach terminal restriction fragment length polymorphism (T-RFLP), in combination with 16S rRNA gene cloning and sequencing. T-RFLP analysis revealed a complex bacterial community in the cancer patients that was not significantly different from that in the controls. Sequencing of 140 clones revealed 102 phylotypes, with representatives from five bacterial phyla (Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria and Fusobacteria). The data revealed a relatively low abundance of H. pylori and showed that the gastric cancer microbiota was instead dominated by different species of the genera Streptococcus, Lactobacillus, Veillonella and Prevotella. The respective role of these species in development of gastric cancer remains to be determined.
Dicksved
Johan
J
Department of Microbiology, Swedish University of Agricultural Sciences, Uppsala, Sweden.
Lindberg
Mathilda
M
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden.|Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden.
Rosenquist
Magnus
M
Department of Oncology, Radiology and Clinical Immunology, Uppsala University Hospital, 751 85 Uppsala, Sweden.
Enroth
Helena
H
Department of Clinical Microbiology, Unilabs AB, Kärnsjukhuset, Skövde, Sweden.
Jansson
Janet K
JK
Lawrence Berkeley National Laboratory, Division of Earth Sciences, Berkeley, CA, USA.|Department of Microbiology, Swedish University of Agricultural Sciences, Uppsala, Sweden.
Engstrand
Lars
L
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, 171 77 Stockholm, Sweden.|Swedish Institute for Infectious Disease Control, 171 82 Solna, Sweden.
D000368:Aged; D000369:Aged, 80 and over; D001419:Bacteria / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification*; D016022:Case-Control Studies; D003001:Cloning, Molecular; D004269:DNA, Bacterial / Q000737:chemistry; D005260:Female; D015723:Gene Library; D006801:Humans; D008297:Male; D008875:Middle Aged; D010802:Phylogeny; D012150:Polymorphism, Restriction Fragment Length; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D013270:Stomach / Q000382:microbiology*; D013274:Stomach Neoplasms / Q000382:microbiology*
D004269:DNA, Bacterial; D012336:RNA, Ribosomal, 16S