Mucosal microbial microenvironment in early gastric neoplasia and non‐neoplastic gastric disease

Abstract

Background and Aim The biological characterization of microbial environment in early gastric cancer (EGC), other than Helicobacter pylori, is limited. This study aimed to explore the microbial microenvironment in chronic gastritis (CG), fundic gland polyps (FGPs), low‐grade intraepithelial neoplasia (LGIN), and EGC. Methods 16S‐rRNA gene sequencing and bioinformatic analysis were performed on 63 individuals with 252 mucosal biopsies or endoscopic submucosal dissection margin samples from endoscopy. Results The microbiota in gastric LGIN functions analogously to EGC in terms of functional prediction. Neoplastic lesions showed a significant difference to CG or FGPs in beta diversity of the microbiota. Bacteria genera including Paracoccus, Blautia, Barnesiella, Lactobacillus, Thauera, Collinsella were significantly enriched in gastric neoplastic mucosa (LGIN and EGC) compared with non‐neoplastic tissues (CG and FGPs). While Pseudomonas and Kingella were depleted in neoplastic tissues. FGPs showed a distinctive microbial network system that negatively interacted with Helicobacter. Conclusions In terms of the mucosal microbial microenvironment, gastric LGIN and EGC showed no significant difference as early neoplastic lesions. We observed a coordinated microbial microenvironment that correlated negatively with Helicobacter.

Alteration of gut microbiome and correlated amino acid metabolism are associated with acute myelocytic leukemia carcinogenesis

“…These results revealed the significant different profiles of gut microbiota derived from AML patients and patients treated with chemotherapy or healthy subjects. Similarly, the genera Collinsella was found to be enriched in several malignant tumors, such as colorectal cancer, 36 gastric cancer, 37 esophageal cancer, 38 and hematological malignant 39 …”

Lipopolysaccharide exacerbates to the migration, invasion, and epithelial‐mesenchymal transition of esophageal cancer cells by TLR4/NF‐κB axis

“…The colonization of ST11 K. pneumoniae significantly promoted the growth and progression of colorectal adenomas in a colitis‐associated mouse model 31 . Collinsella as a conditional pathogenic bacterium, was reported to be significantly enriched in gastric neoplastic mucosa compared with nonneoplastic tissues and show potential to differentiate gastric cancer stages 32 . A significantly increased abundance of Collinsella was observed in stool of EC patients 8 .…”

“…31 Collinsella as a conditional pathogenic bacterium, was reported to be significantly enriched in gastric neoplastic mucosa compared with nonneoplastic tissues and show potential to differentiate gastric cancer stages. 32 A significantly increased abundance of Collinsella was observed in stool of EC patients. 8 The role of Collinsella in EC progression remains to be explored.…”

Gastric microbiota and its role in gastric carcinogenesis

“…At the genus level, Peptostreptococcus , Comamonadaceae , Mogibacterium , and Gemella were also more represented in GC than in other gastric lesions or adjacent noncancerous tissues [47, 54]. The genus of Lactobacillus and family of Lachnospiraceae showed higher abundance in GC patients compared to patients with other stages of gastric lesion [24, 64, 68, 74, 75]. Several studies also indicated that Clostridium is often colonized in the gastric mucosa of GC patients [24, 76].…”