The Roles of Intrahepatic Vα14+ Nk1.1+ T Cells for Liver Injury Induced By Salmonella Infection in Mice

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Abstract
To investigate the roles of intrahepatic T cells in liver injury after Salmonella infection, we examined serum alanine transaminase (ALT), histopathology, and bacterial numbers in liver after infection with Salmonella choleraesuis strain 31N–1 in mice genetically lacking TCRαβ+, CD4+, CD8+, or NK1.1+T cells with C57BL/6 background. In control (+/+) mice, serum ALT reached a peak level by day 7 after an intraperitoneal inoculation of 2 × 106 CFU Salmonella choleraesuis 31N–1. In TCR–β-/- mice, liver injury, as assessed by serum ALT level and histological examination, was significantly suppressed on day 7 after Salmonella infection but the numbers of bacteria in liver did not differ from those in normal mice, suggesting that αβ T cells are responsible for liver injury induced by Salmonella infection. To further determine which subsets in αβ T cells are important for the liver injury, we compared serum ALT level in mice genetically lacking CD4, CD8, β2–microglobulin (β2m, IAβ, or Jα281 after Salmonella infection. In CD4-/- mice, serum ALT was significantly lower in comparison with control mice, but there was no difference in serum ALT levels in CD8-/- and IAβ-/- mice from that in control mice. Notably, serum ALT levels and pathological lesions in liver were significantly decreased in β2m-/- or Jα281-/- mice, which lacked in NK1.1+ T cells bearing TCR Vα14–Jα281 specific for β2m–associated CD1d, following Salmonella infection. Taken together, it is suggested that αβ T cells bearing NK1.1 and CD4 may be main effector cells for liver injury after Salmonella infection.