Salmonella transforms follicle-associated epithelial cells into M cells to promote intestinal invasion

Amin Tahoun, Simmi Mahajan, Edith Paxton, Georg Malterer, David S Donaldson, Dai Wang, Alwyn Tan, Trudi L Gillespie, Marie O'Shea, Andrew J Roe, Darren J Shaw, David L Gally, Andreas Lengeling, Neil A Mabbott, Juergen Haas, Arvind Mahajan

Research output: Contribution to journalArticlepeer-review


Salmonella Typhimurium specifically targets antigen-sampling microfold (M) cells to translocate across the gut epithelium. Although M cells represent a small proportion of the specialized follicular-associated epithelium (FAE) overlying mucosa-associated lymphoid tissues, their density increases during Salmonella infection, but the underlying molecular mechanism remains unclear. Using in vitro and in vivo infection models, we demonstrate that the S. Typhimurium type III effector protein SopB induces an epithelial-mesenchymal transition (EMT) of FAE enterocytes into M cells. This cellular transdifferentiation is a result of SopB-dependent activation of Wnt/β-catenin signaling leading to induction of both receptor activator of NF-κB ligand (RANKL) and its receptor RANK. The autocrine activation of RelB-expressing FAE enterocytes by RANKL/RANK induces the EMT-regulating transcription factor Slug that marks epithelial transdifferentiation into M cells. Thus, via the activity of a single secreted effector, S. Typhimurium transforms primed epithelial cells into M cells to promote host colonization and invasion.
Original languageEnglish
Pages (from-to)645-56
Number of pages12
JournalCell Host & Microbe
Issue number5
Publication statusPublished - 2012


Dive into the research topics of 'Salmonella transforms follicle-associated epithelial cells into M cells to promote intestinal invasion'. Together they form a unique fingerprint.

Cite this