Lawsonia intracellularis is a recently identified bacterial pathogen which causes disease in a broad range of animals. Invasion of intestinal epithelial cells and the resultant
hyperplasia of infected cells are central processes in disease pathogenesis. In this study, we aimed to establish whether immunocompetent mice were susceptible to
infection and whether
gamma interferon (IFN-gamma) contributed to the pathogenesis of
infection. Wild-type 129-Sv-Ev mice (129 mice) and IFN-gamma receptor knockout mice based on the 129 background (
IFN-gammaR(-)) were challenged orally with approximately 5.5 x 10(7) L. intracellularis cells. Both 129 and
IFN-gammaR(-) mice became infected, although the extent of
infection (as determined by the proportion of infected crypts) was substantially lower in 129 mice than in
IFN-gammaR(-) mice. Despite these differences, infected crypts showed characteristics typical of proliferative enteropathies of other animals, i.e., intracellular colonization of epithelial cells by L. intracellularis with resultant epithelial
hyperplasia.
Infection in 129 mice was cleared between days 21 and 28 postchallenge, whereas
infection in
IFN-gammaR(-) mice was evident in 100% of animals from day 21 onward. Additionally, in
IFN-gammaR(-) mice the
infection was so extensive that fatalities resulted. IFN-gamma therefore plays a significant role in limiting intracellular
infection and increased cellular proliferation associated with L. intracellularis. L. intracellularis
infection is generally associated with modest cellular infiltration; therefore, further comparative examinations will be necessary to determine
pathogenicity factors and define the role of IFN-gamma in controlling this
infection.