Rapid reversal of interleukin-6-dependent epithelial invasion in a mouse model of microbially induced colon carcinoma (original) (raw)

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5 Present address: Laboratory of Pathology, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki, Thessaloniki 54006, Greece

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2 Center for Cancer Research, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA

6 Present address: Unit for Molecular Pathology, Center for Cancer Research, Massachusetts General Hospital, Bldg 149, Rm 7148, 13th Street, Charlestown, MA 02129, USA

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3 Department of Medicine and Microbiology, Columbia University, 1130 St Nicholas Avenue, Room 918, New York, NY 10032

7 Present address: Feinstein Institute for Medical Research, 350 Community Drive, Manhasset NY 11030, USA

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4 Immunology Research Division, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA

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Revision received:

26 July 2007

Published:

27 August 2007

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Theofilos Poutahidis, Kevin M. Haigis, Varada P. Rao, Prashant R. Nambiar, Christie L. Taylor, Zhongming Ge, Koichiro Watanabe, Anne Davidson, Bruce H. Horwitz, James G. Fox, Susan E. Erdman, Rapid reversal of interleukin-6-dependent epithelial invasion in a mouse model of microbially induced colon carcinoma, Carcinogenesis, Volume 28, Issue 12, December 2007, Pages 2614–2623, https://doi.org/10.1093/carcin/bgm180
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Abstract

Chronic inflammation of mucosal surfaces renders them increasingly susceptible to epithelial cancers both in humans and mice. We have previously shown that anti-inflammatory CD4 + CD45RB lo CD25 + regulatory (Treg or T R ) lymphocytes down-regulate inflammation and block development of bacteria-triggered colitis and colorectal cancer (CRC) in 129/SvEv Rag2−/− mice. Interestingly, T R cells collected from Interleukin (IL)-10-deficient cell donors not only failed to suppress carcinogenesis but instead promoted invasive mucinous colonic carcinoma with a strong gender bias expressing in male mice. We found we show that peritoneal invasion in this model is dependent on pleiotropic cytokine IL-6. Mucinous carcinoma arose rapidly and consistently after treatment with IL10−/− T R cells, which were found to express Foxp3+ and localize throughout tumor tissue. Carcinogenesis was rapidly reversible with transfer of wild type IL10-competent T R cells. Likewise, treatment with IL10-Ig fusion protein was sufficient to revert the lesions histologically, and restore inflammatory cytokine and oncogene expression to base line levels. These studies indicate an essential role for IL 6 in this CRC phenotype. Furthermore, immune-competent T R cells were important not only for preventing pathology but also for constructive remodeling of bowel following tumorigenic microbial insults. These data provide insights into etiopathogenesis of inflammation-associated epithelial invasion and maintenance of epithelial homeostasis.

© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Topic:

• cytokine
• phenotype
• cancer
• carcinoma
• epithelium
• homeostasis
• fusion proteins
• colitis
• interleukin-10
• interleukins
• lymphocytes
• oncogenes
• immunoglobulins
• bacteria
• colon
• interleukin-6
• mice
• neoplasms
• antigens, cd25

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