Table 1 Potential microbial species that are involved in the promotion or inhibition of progression in pancreatic cancer
From: Microbiome as a biomarker and therapeutic target in pancreatic cancer
Biomarker | Site | Proposed Mechanisms | Effects | Ref. |
|---|---|---|---|---|
Porphyromonas gingivalis | Mouth | Elevation of the neutrophilic chemokine and neutrophil elastase secretion | promotes pancreatic cancer progression in vivo | [48] |
Porphyromonas gingivalis | Mouth | initiate the Toll-like receptor signaling pathways; Evasion of the host immune system by invasion of host cells and disruption of signaling pathways by cytokine and receptor degradation; | Higher risk of pancreatic cancer | [57] |
Aggregatibacter actinomycetemcomitans | Mouth | initiate the Toll-like receptor signalling pathways | Twofold increase in PDAC risk | [57] |
Phylum Fusobacteria and genus Leptotrichia | Mouth | Immune response elicited by Leptotrichia may provide protection against pancreatic carcinogenesis | Lower risk of developing PC | [57] |
Fusobacterium nucleatum | Intratumoral cells (In vitro) | Induced both normal pancreatic epithelial cells and PDAC cells to secrete increased amounts of the cytokines GM-CSF, CXCL1, IL-8, and MIP-3α | infection in both normal pancreatic epithelial cells and PDAC cells caused an increase in cytokine secretion, promoting phenotypes in PDAC cells associated with tumor progression | [58] |
Streptococcus and Leptotrichina | Mouth | NA | Increased risk of PDAC development | [59] |
Veillonella and Neisseria | Mouth | NA | Decreased risk of PDAC and promotion of protective characteristics | [59] |
Porphyromonas, Fusobacterium, and Alloprevotella | Mouth | NA | Seen in patients reporting bloating | [59] |
Prevotella | Mouth | NA | Greater abundance in patients with jaundice | [59] |
Veillonella | Mouth | NA | Greater abundance in patients with dark brown urine | [59] |
Neisseria and Campylobacter | Mouth | NA | Lower amounts in patients with diarrhea | [59] |
Alloprevotella | Mouth | NA | Lowe amounts in patients with vomiting | [59] |
Fusobacterium nucleatum subsp. vincentii and Gemella morbillorum | Oral, Intestinal, Pancreatic | Oral bacteria can pass through the oral mucosal barrier, result in abnormal local and systemic immune and metabolic responses | Specific co-abundance patterns in oral and intestinal or pancreatic samples | [60] |
Bifidobacterium | Intestinal (Duodenal fluid) | PPIs can lead to bacterial shifts and the increase of pathogenic bacteria | Increased in PDAC patients | [62] |
Fusobacteria and Rothia | Intestinal (Duodenal fluid) | PPIs can lead to bacterial shifts and the increase of pathogenic bacteria | Higher levels related with short-term survival (STS) | [62] |
Lactobacillus, Haemophilus, and Streptococcus | Intestinal (Stool) | gut microbial functions involved in Leucine and LPS biosynthesis enriched, while Spermidine putrescine transport system and Histidine biosynthesis reduced in PC, leading to chronic inflammation | More abundant in stage II PC patients | [64] |
Streptococcus | Intestinal (Stool) | Streptococcus is associated with bile acid and lipid homeostasis in the gut | More notable in PCH compared with PCB and significant elevation in PCH-O versus PCH-unO | [64] |
Akkermansia | Bile fluid | Akkermansia is associated with the performance of external biliary drainage | More likely to be detected in patients with biliary tract cancer and external biliary drainage | [65] |
Pseudoxanthomonas, Streptomyces, Saccharopolyspora, and Bacillus clausii | Tumor tissue | Tumor microbiome shapes immune responses promoting T cell activation | Intra-tumoral microbiome signature in long-term survival (LTS) patients | [44] |
Gammaproteobacteria and Bacilli | Cyst fluid after resection | By inducing pancreatic cell damage including DNA repair response and cell death | Dominant in pancreatic cyst fluid in intraductal papillary mucinous neoplasm | [66] |
A. baumannii and M. hyopneumoniae | Tumor tissue | part of a pathway for tobacco to influence disease severity | Associated with smoking that cause genomic changes leading to PDAC | [67] |
A. ebreus, A. baumannii, G. kaustophilus, and E. coli | Tumor tissue | Increase cancer activation and immune-suppression pathways in males compared to females | Differential abundance and activation of cancer and immune-associated pathways in male versus female pancreatic adenocarcinoma patients | [67] |
Citrobacter freundii, Pseudomonadales bacterium, A. ebreus | Tumor tissue | Proinflammatory immune pathway activation | Upregulation of oncogenic pathways | [67] |
Malassezia spp. | Tumor tissue | Ligation of mannose-binding lectin (MBL) required for oncogenic progression | Malassezia was enriched in pancreatic ductal adenocarcinoma in both mice and humans | [69] |
Candida | Oral | Inhabits on the mucosal epithelium and causes various oral mucosal lesions; Exerts carcinogenetic effects through production of carcinogenic byproducts, triggering inflammation, induction of the Th17 response and through molecular mimicry | Increased risk of developing pancreatic cancer in individuals with Candida-related oral mucosal lesions | |
Hepatitis C virus | NA | Increased risk of diabetes and elevated pancreatic enzymes; HCV proteins interact with components of cytoplasmatic enzymes and cell cytoskeleton leading to dysregulation of transcriptional cell genome activities | Elevated risk of PC | [74] |
P. gingivalis | Oral | TGF-β signaling pathway may be involved in the cancer-promoting effect of P. gingivalis and the suppressive effects of probiotics | Accelerated development of PanIN lesions in oral exposure | [138] |
Pathogenic E. coli | Intestinal | Can activate the TUBB/Rho/ROCK signaling pathway | participates in the carcinogenesis of pancreatic cancer. | [155] |