Previous Article | Next Article ![]()
Infection and Immunity, March 2004, p. 1645-1656, Vol. 72, No. 3
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.3.1645-1656.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Peter H. Dube,1,
,
Paula A. Revell,1,
and Virginia L. Miller1,2*
Department of Molecular Microbiology,1 Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri 631102
Received 16 May 2003/ Returned for modification 18 July 2003/ Accepted 8 December 2003
Several studies have highlighted differences in the resistances of various mouse strains to intravenous (i.v.) infection with Yersinia enterocolitica. In particular, differences in resistance and immunological response between BALB/c and C57BL/6 mouse strains have been determined. Following i.v infection, C57BL/6 mice are more resistant to Y. enterocolitica than are BALB/c mice. However, because Y. enterocolitica is typically a food-borne pathogen, the oral route of infection more accurately reflects the natural route of infection. Therefore, it was of interest to ascertain if the differences in resistance between mouse strains observed for an i.v. infection can be recapitulated following an oral infection. C57BL/6j, BALB/cj, and 129X1/Svj mouse strains presented no differences in 50% lethal dose (LD50) following oral infection with Y. enterocolitica. Subsequent analysis of cytokine levels, bacterial colonization and immune cell populations following oral infection confirmed characteristics previously described following i.v. Y. enterocolitica infection. All tissues analyzed from each mouse strain demonstrated a polarized Th1 cytokine profile and inflammatory cell influx throughout a 7-day course of infection. This immune response was present in all tissues and increased as bacterial colonization progressed. The lack of a differing LD50 phenotype and common trends in immunological response among the three mouse strains tested suggests that oral infection is a useful model for studying the host response to Y. enterocolitica infection.
S.A.H. and P.H.D. contributed equally to this work.
Present address: Department of Microbiology and Immunology, University of Texas Health Sciences Center at San Antonio, San Antonio, TX 78229-3900.
Present address: Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»