Table 2. Flora alterations in gut microbiota and proposed dysbiotic mechanisms promoting tumorigenesis.
| Condition | Associated flora | Proposed mechanisms inducing pathology | References |
|---|---|---|---|
| Normal esophagus | Streptococcus, Prevotella, Rothia, Hemophilus, Fusobacterium, TM7/Saccharibacteria | – | (34,35) |
| Barrett’s esophagus, esophageal adenocarcinoma | ↑gram-negative flora, ↓Streptococcus | ↑lactic acid production → chronic inflammation; activation of LPS-TLR-NF-κB pathway → chronic inflammation | (35-41) |
| ↑Lactobacillus | ↑lactic acid production → chronic inflammation | ||
| Esophageal squamous cell cancer | ↓microbial diversity; alterations in adjacent microbiota (oral, gastric corpus) | – | (42-47) |
| ↑Porphyromonas gingivalis | Activation of Jak1/Akt/Stat3 pathway → dysregulation of apoptosis; conversion of ethanol to acetaldehyde → genotoxin formation | ||
| ↑Fusobacterium nucleatum | ↑CCL20 chemokine production → dysregulated immune surveillance | ||
| – | Degradation of epithelial basement membrane via MMP release, induction of DAMPs → chronic inflammation | ||
| Normal stomach | Streptococcus, Lactobacillus, Veillonella, Prevotella, Rothia, Neisseria | – | (48) |
| Gastric carcinoma | Pathogenic strains of Helicobacter pylori | NF-κB pathway mediated cytokine release → chronic inflammation, dysregulation of apoptosis | (47-52) |
| – | CagA oncoprotein activation of Ras-Erk mitogenic pathway → disruption of host cellular signaling; VacA oncoprotein induced host cell destruction → chronic inflammation | ||
| Pathobiont overgrowth promoted by Helicobacter pylori | Urease allows neutralization of acidic environment and reaction with neutrophilic metabolites → genotoxin formation | ||
| ↑Lactobacillus, Lachnospiraceae, Burkholderia, Escheria, Shigella | ↑N-nitroso compound metabolism → genotoxin formation | ||
| ↑Lactobacillus, Lactococcus | ↑lactic acid production → chronic inflammation |
LPS-TLR-NF-κB, lipopolysaccharide-toll-like receptor-nuclear factor-kappa beta; CCL20, C-C chemokine ligand 20; DAMP, danger associated membrane proteins.