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Infection and Immunity, August 2007, p. 3802-3811, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.00419-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Yersinia enterocolitica Infection of Mice Reveals Clonal Invasion and Abscess Formation{triangledown}

Mark F. Oellerich,{dagger} Christoph A. Jacobi,{dagger} Sandra Freund, Katy Niedung, Alexandra Bach, Jürgen Heesemann, and Konrad Trülzsch*

Max von Pettenkofer Institute for Hygiene and Medical Microbiology, Ludwig Maximillians University, D-80336 Munich, Germany

Received 21 March 2007/ Returned for modification 7 May 2007/ Accepted 25 May 2007

Yersinia enterocolitica is a common cause of food-borne gastrointestinal disease leading to self-limiting diarrhea and mesenteric lymphadenitis. Occasionally, focal abscess formation in the livers and spleens of certain predisposed patients (those with iron overload states such as hemochromatosis) is observed. In the mouse oral infection model, yersiniae produce a similar disease involving the replication of yersiniae in the small intestine, the invasion of Peyer's patches, and dissemination to the liver and spleen. In these tissues and organs, yersiniae are known to replicate predominately extracellularly and to form microcolonies. By infecting mice orally with a mixture of equal amounts of green- and red-fluorescing yersiniae (yersiniae expressing green or red fluorescent protein), we were able to show for the first time that yersiniae produce exclusively monoclonal microcolonies in Peyer's patches, the liver, and the spleen, indicating that a single bacterium is sufficient to induce microcolony and microabscess formation in vivo. Furthermore, we present evidence for the clonal invasion of Peyer's patches from the small intestine. The finding that only very few yersiniae are required to establish microcolonies in Peyer's patches is due to both Yersinia-specific and host-specific factors. We demonstrate that yersiniae growing in the small intestinal lumen show strongly reduced levels of invasin, the most important factor for the early invasion of Peyer's patches. Furthermore, we show that the host severely restricts sequential microcolony formation in previously infected Peyer's patches.


* Corresponding author. Mailing address: Max von Pettenkofer Institute for Hygiene and Medical Microbiology, Ludwig Maximillians University, Pettenkoferstrasse 9a, 80336 München, Germany. Phone: (49-89) 51605279. Fax: (49-89) 51605223. E-mail: truelzsch{at}mvp.uni-muenchen.de

{triangledown} Published ahead of print on 11 June 2007.

Editor: J. B. Bliska

{dagger} These authors contributed equally to this work.


Infection and Immunity, August 2007, p. 3802-3811, Vol. 75, No. 8
0019-9567/07/$08.00+0     doi:10.1128/IAI.00419-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




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