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Pathogenic intestinal bacteria enhance prostate cancer development via systemic activation of immune cells in mice.

Authors :
Theofilos Poutahidis
Kelsey Cappelle
Tatiana Levkovich
Chung-Wei Lee
Michael Doulberis
Zhongming Ge
James G Fox
Bruce H Horwitz
Susan E Erdman
Source :
PLoS ONE, Vol 8, Iss 8, p e73933 (2013)
Publication Year :
2013
Publisher :
Public Library of Science (PLoS), 2013.

Abstract

A role for microbes has been suspected in prostate cancer but difficult to confirm in human patients. We show here that a gastrointestinal (GI) tract bacterial infection is sufficient to enhance prostate intraepithelial neoplasia (PIN) and microinvasive carcinoma in a mouse model. We found that animals with a genetic predilection for dysregulation of wnt signaling, Apc (Min/+) mutant mice, were significantly susceptible to prostate cancer in an inflammation-dependent manner following infection with Helicobacter hepaticus. Further, early neoplasia observed in infected Apc (Min/+) mice was transmissible to uninfected mice by intraperitoneal injection of mesenteric lymph node (MLN) cells alone from H. hepaticus-infected mutant mice. Transmissibility of neoplasia was preventable by prior neutralization of inflammation using anti-TNF-α antibody in infected MLN donor mice. Taken together, these data confirm that systemic inflammation triggered by GI tract bacteria plays a pivotal role in tumorigenesis of the prostate gland.

Subjects

Subjects :
Medicine
Science

Details

Language :
English
ISSN :
19326203
Volume :
8
Issue :
8
Database :
Directory of Open Access Journals
Journal :
PLoS ONE
Publication Type :
Academic Journal
Accession number :
edsdoj.9e65dfe39b14b018866182300b7032e
Document Type :
article
Full Text :
https://doi.org/10.1371/journal.pone.0073933