Possible involvement of Enterococcus infection in the pathogenesis of chronic pancreatitis and cancer

Maekawa, Toshiro; Fukaya, Risako; Takamatsu, Shinji; Itoyama, Saki; Fukuoka, Tetsuo; Yamada, Makoto; Hata, Tomoki; Nagaoka, Satoshi; Kikuchi, Kôichi; Eguchi, Hidetoshi; Murata, Kohei; Kumada, Takashi; Ito, Toshifumi; Tanemura, Masahiro; Fujimoto, K; Tomita, Yoshihiro; Tobe, Toru; Kamada, Y.; Miyoshi, Eiji

doi:10.1016/j.bbrc.2018.10.169

Cited by 85 publications

(82 citation statements)

References 16 publications

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“…Furthermore, another interesting aspect that requires investigation would be the divergent effects of IL-22 signaling in organs that are traditionally considered to be sterile. A specific example of this would be in the pancreas [ 136 ], where IL-22 is known to promote repair and renewal of pancreatic acinar cells during injury [ 137 ], but may also lead to the development of pancreatic carcinoma when dysregulated [ 138 ]. Recent findings have shown an increase of bacteria in pancreatic carcinoma patients [ 139 , 140 ].…”

Section: Discussionmentioning

confidence: 99%

Microbiota-Dependent Effects of IL-22

Sabihi

Böttcher

Pelczar

et al. 2020

Cells

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Cytokines are important contributors to immune responses against microbial and environmental threats and are of particular importance at epithelial barriers. These interfaces are continuously exposed to external factors and thus require immune components to both protect the host from pathogen invasion and to regulate overt inflammation. Recently, substantial efforts have been devoted to understanding how cytokines act on certain cells at barrier sites, and why the dysregulation of immune responses may lead to pathogenesis. In particular, the cytokine IL-22 is involved in preserving an intact epithelium, maintaining a balanced microbiota and a functioning defense system against external threats. However, a tight regulation of IL-22 is generally needed, since uncontrolled IL-22 production can lead to the progression of autoimmunity and cancer. Our aim in this review is to summarize novel findings on IL-22 and its interactions with specific microbial stimuli, and subsequently, to understand their contributions to the function of IL-22 and the clinical outcome. We particularly focus on understanding the detrimental effects of dysregulated control of IL-22 in certain disease contexts.

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Section: Discussionmentioning

confidence: 99%

Microbiota-Dependent Effects of IL-22

Sabihi

Böttcher

Pelczar

et al. 2020

Cells

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“…In the oral microbiome, Porphyromonas gingivalis increased in pancreatic adenocarcinoma [64,82,83,85,101]. Helicobacter pylori [62,69,70], Enterobacter, Enterococcus [64,90,92,93], Fusobacteria [89,94,102], and E. coli [64,93] were also shown to increase in pancreatic adenocarcinoma patients in multiple studies. In a study assessing intratumor DNA and serum cell-free DNA (1000+ patients), Fusobacteria count in tumors was higher compared to the healthy, untransformed tissues [102].…”

Section: The Oncobiome In Pancreatic Adenocarcinomamentioning

confidence: 97%

“…Characteristic changes occur to the oral [63,[81][82][83][84][85][86][87][88] and duodenal microbiome [64] in pancreatic adenocarcinoma. Enterobacter, Enterococcus, and E. coli bactibilia [78] or the colonization of the pancreas [41,65,68,[89][90][91][92][93][94] are risk factors for pancreatic adenocarcinoma. Of note, an oncogenic role of hepatotropic viruses (Hepatitis B and C virus and Transfusion Transmitted/Torque Teno virus) in pancreatic adenocarcinoma has been observed in a clinical setting, although the exact molecular mechanisms are yet unknown [78].…”

Section: The Oncobiome In Pancreatic Adenocarcinomamentioning

confidence: 99%

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Oncobiosis and Microbial Metabolite Signaling in Pancreatic Adenocarcinoma

Kiss

Mikó

Sebő³

et al. 2020

Cancers

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Pancreatic adenocarcinoma is one of the most lethal cancers in both men and women, with a median five-year survival of around 5%. Therefore, pancreatic adenocarcinoma represents an unmet medical need. Neoplastic diseases, such as pancreatic adenocarcinoma, often are associated with microbiome dysbiosis, termed oncobiosis. In pancreatic adenocarcinoma, the oral, duodenal, ductal, and fecal microbiome become dysbiotic. Furthermore, the pancreas frequently becomes colonized (by Helicobacter pylori and Malassezia, among others). The oncobiomes from long- and short-term survivors of pancreatic adenocarcinoma are different and transplantation of the microbiome from long-term survivors into animal models of pancreatic adenocarcinoma prolongs survival. The oncobiome in pancreatic adenocarcinoma modulates the inflammatory processes that drive carcinogenesis. In this review, we point out that bacterial metabolites (short chain fatty acids, secondary bile acids, polyamines, indole-derivatives, etc.) also have a role in the microbiome-driven pathogenesis of pancreatic adenocarcinoma. Finally, we show that bacterial metabolism and the bacterial metabolome is largely dysregulated in pancreatic adenocarcinoma. The pathogenic role of additional metabolites and metabolic pathways will be identified in the near future, widening the scope of this therapeutically and diagnostically exploitable pathogenic pathway in pancreatic adenocarcinoma.

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“…352 Patients with pancreatic cancer and chronic pancreatitis are characterized by increased serum levels of antibodies against the capsular polysaccharide of Enterococcus faecalis (E. faecalis) compared with healthy volunteers, suggesting that infection with E. faecalis is involved in the development of pancreatitisassociated cancer. 355 Similarly, another study that conducted a microbiological investigation of bile from female patients with pancreas head carcinoma (PHC) showed a remarkably positive correlation between the abundance of Bactibilia and PHC.…”

Section: Zhang Et Almentioning

confidence: 99%

Demystifying the manipulation of host immunity, metabolism, and extraintestinal tumors by the gut microbiome

Zhang

Tang

Chen

et al. 2019

Sig Transduct Target Ther

191

151

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The trillions of microorganisms in the gut microbiome have attracted much attention recently owing to their sophisticated and widespread impacts on numerous aspects of host pathophysiology. Remarkable progress in large-scale sequencing and mass spectrometry has increased our understanding of the influence of the microbiome and/or its metabolites on the onset and progression of extraintestinal cancers and the efficacy of cancer immunotherapy. Given the plasticity in microbial composition and function, microbial-based therapeutic interventions, including dietary modulation, prebiotics, and probiotics, as well as fecal microbial transplantation, potentially permit the development of novel strategies for cancer therapy to improve clinical outcomes. Herein, we summarize the latest evidence on the involvement of the gut microbiome in host immunity and metabolism, the effects of the microbiome on extraintestinal cancers and the immune response, and strategies to modulate the gut microbiome, and we discuss ongoing studies and future areas of research that deserve focused research efforts.

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Possible involvement of Enterococcus infection in the pathogenesis of chronic pancreatitis and cancer

Cited by 85 publications

References 16 publications

Microbiota-Dependent Effects of IL-22

Microbiota-Dependent Effects of IL-22

Oncobiosis and Microbial Metabolite Signaling in Pancreatic Adenocarcinoma

Demystifying the manipulation of host immunity, metabolism, and extraintestinal tumors by the gut microbiome

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