Pathogenic Intestinal Bacteria Enhance Prostate Cancer Development via Systemic Activation of Immune Cells in Mice
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Poutahidis-2013-Pathogenic Intestina.pdf
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Author(s)
Poutahidis, Theofilos
Cappelle, Kelsey
Levkovich, Tatiana
Lee, Chung-Wei
Doulberis, Michael
Ge, Zhongming
Fox, James G.
Horwitz, Bruce H.
Erdman, Susan E.
Date Issued
August 2013
Journal
PLoS ONE
Publisher
Public Library of Science
Citation
Poutahidis, Theofilos, Kelsey Cappelle, Tatiana Levkovich, Chung-Wei Lee, Michael Doulberis, Zhongming Ge, James G. Fox, Bruce H. Horwitz, and Susan E. Erdman. “Pathogenic Intestinal Bacteria Enhance Prostate Cancer Development via Systemic Activation of Immune Cells in Mice.” Edited by Deyu Fang. PLoS ONE 8, no. 8 (August 26, 2013): e73933.
Version
Final published version
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[superscript 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[superscript 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.
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Massachusetts Institute of Technology. Division of Comparative Medicine
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DOI of Published Version
https://doi.org/10.1371/journal.pone.0073933
