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*
Department of Biochemistry, Center for Molecular Microbiology and Infection, Imperial College, South Kensington, London, United Kingdom;
Division of Infection, Inflammation, and Repair, University of Southampton School of Medicine, Southampton, United Kingdom; and
Department of Adult and Pediatric Gastroenterology, St. Bartholomew’s and Royal London School of Medicine and Dentistry, London, United Kingdom
Mice infected with Citrobacter rodentium represent
an excellent model in which to examine immune defenses against an
attaching-effacing enteric bacterial pathogen. Colonic tissue from mice
infected with C. rodentium harbors increased transcripts
for IL-12 and IFN-
and displays mucosal pathology compared with
uninfected controls. In this study, the role of IL-12 and IFN- in
host defense and mucosal injury during C. rodentium
infection was examined using gene knockout mice.
IL-12p40-/- and IFN--/- mice were
significantly more susceptible to mucosal and gut-derived systemic
C. rodentium infection. In particular, a proportion of
IL-12p40-/- mice died during infection. Analysis of the
gut mucosa of IL-12p40-/- mice revealed an influx of
CD4+ T cells and a local IFN- response. Infected
IL-12p40-/- and IFN--/- mice also
mounted anti-Citrobacter serum and gut-associated
IgA responses and strongly expressed inducible NO synthase (iNOS) in
mucosal tissue, despite diminished serum nitrite/nitrate levels.
However, iNOS does not detectably contribute to host defense against
C. rodentium, as iNOS-/- mice were not
more susceptible to infection. However, C57BL/6 mice infected with
C. rodentium up-regulated expression of the mouse
-defensin (mBD)-1 and mBD-3 in colonic tissue. In contrast,
expression of mBD-3, but not mBD-1, was significantly attenuated during
infection of IL-12- and IFN--deficient mice, suggesting mBD-3 may
contribute to host defense. These studies are among the first to
examine mechanisms of host resistance to an attaching-effacing pathogen
and show an important role for IL-12 and IFN- in limiting bacterial
infection of the colonic epithelium.
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