The myeloid immune signature of enterotoxigenic Bacteroides fragilis-induced murine colon tumorigenesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-03

AUTHORS

Erik Thiele Orberg, Hongni Fan, Ada J. Tam, Christine M. Dejea, Christina E. Destefano-Shields, Shaoguang Wu, Liam Chung, Benjamin B. Finard, Xinqun Wu, Payam Fathi, Sudipto Ganguly, Juan Fu, Drew M. Pardoll, Cynthia L. Sears, Franck Housseau

ABSTRACT

Enterotoxigenic Bacteroides fragilis (ETBF), a human commensal and candidate pathogen in colorectal cancer (CRC), is a potent initiator of interleukin-17 (IL-17)-dependent colon tumorigenesis in MinApc+/- mice. We examined the role of IL-17 and ETBF on the differentiation of myeloid cells into myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages, which are known to promote tumorigenesis. The myeloid compartment associated with ETBF-induced colon tumorigenesis in Min mice was defined using flow cytometry and gene expression profiling. Cell-sorted immature myeloid cells were functionally assayed for inhibition of T-cell proliferation and inducible nitric oxide synthase expression to delineate MDSC populations. A comparison of ETBF infection with that of other oncogenic bacteria (Fusobacterium nucleatum or pks+Escherichia coli) revealed a specific, ETBF-associated colonic immune infiltrate. ETBF-triggered colon tumorigenesis is associated with an IL-17-driven myeloid signature characterized by subversion of steady-state myelopoiesis in favor of the generation of protumoral monocytic-MDSCs (MO-MDSCs). Combined action of the B. fragilis enterotoxin BFT and IL-17 on colonic epithelial cells promoted the differentiation of MO-MDSCs, which selectively upregulated Arg1 and Nos2, produced NO, and suppressed T-cell proliferation. Evidence of a pathogenic inflammatory signature in humans colonized with ETBF may allow for the identification of populations at risk for developing colon cancer. More... »

PAGES

421

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/mi.2016.53

DOI

http://dx.doi.org/10.1038/mi.2016.53

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1036728070

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27301879


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