Review Article

Roles of Commensal Microbiota in Pancreas Homeostasis and Pancreatic Pathologies

Table 2

Microbial species implicated in pancreatic cancer and pancreatitis. A current list of the characterized microbes is shown, which includes the experimental models that were evaluated and the observed effects according to each microbial species. The respective bibliographies are also listed (last column).

Microbial speciesExperimental modelEffectsReferences

N. elongata Saliva samples of PDAC and pancreatitis patientsDecreased in cases[115, 145]

S. mitis Saliva samples of PDAC and pancreatitis patientsDecreased in cases[115, 145]

G. adiacens Saliva samples of PDAC and pancreatitis patientsIncreased in cases[115, 145]

P. gingivalis Blood samples of PDAC patientsHigh levels of antibodies against this species confer higher risk of pancreatic cancer[150]

Commensal oral bacteria Blood samples of PDAC patientsHigh levels of antibodies against this group confer higher risk of pancreatic cancer[150]

H. pylori Blood samples of patients with PDAC, gastric cancer, colorectal cancer, and controlsPancreatic cancer cases had equal risk of H. pylori seropositivity as gastric cancer cases and higher risk than colorectal cancer cases and control[233]
Blood samples of smokers, pancreatic cancer cases, and controlsPatients with exocrine pancreatic cancer had higher rates of seroprevalence for H. pylori [234]
Blood samples of smokers, exocrine pancreatic cancer patients, and controlsH. pylori antigens were not associated with development of pancreatic cancer[135]
Blood sample of newly diagnosed PDAC cases and controlsColonization by H. pylori associated with higher risk of pancreatic cancer, especially for individuals with non-O blood types[235]
Human PDAC cell linesIncreased activities of proliferation factors NF-B, AP-1, and SRE, and secreted higher levels of IL-8 and VEGF[236]

LPSCerulein-induced pancreatitisLPS synergizes with cerulean to induce severe acute pancreatitis[59]
L-Arginine-induced pancreatitisGenetic ablation of TLR4 or CD14 mitigates acute pancreatitis[13]
P48+/Cre; LsL-KRasG12d/+LPS accelerates pancreatic carcinogenesis, TLR4 and TRIF blockade attenuate carcinogenesis, and MyD88 blockade exacerbates carcinogenesis[12]
Ela-CreERT; LsL-KRasG12d/+LPS synergizes with KRas mutation in acinar cells to induce pancreatitis and accelerate pancreatic carcinogenesis[128]