Phenotypic analysis of splenic lymphocytes and immunohistochemical study of hepatic granulomas after a murine infection with Salmonella abortusovis.

Infection in mice with an attenuated strain of Salmonella abortusovis (SAO), a specific pathogen for sheep, was used as a convenient model to understand further the induced immunity against SAO. The hypovirulent Rv6 strain, subcutaneously inoculated in salmonella-susceptible BALB/cby (Itys) mice, colonized the spleen and the liver in less than 6 days post-infection (PI) to be cleared after Day 28 PI. Simultaneously, an increase in spleen cell numbers, splenomegaly and hepatic granulomatous lesions developed to a maximum level on Day 9 PI. In spleen of uninfected mice, the number of Thy-1.2+ cells represents twice the number of surface immunoglobulin-positive cells (sIg+). Cytofluorometric analysis of the spleen lymphoid cell subsets showed a significant increase (10 times, P less than 0.05) in the number of sIg+ cells from Day 6 to Day 28 PI compared to control values. The number of Thy-1.2+ cells also significantly increased, to a lesser degree than the sIg+ cells, on Day 2 and on Day 16 PI (twice control values, P less than 0.05), but decreased on Day 6 PI compared to Day 2 PI. The highest L3T4+:Lyt-2+ ratio was observed on Day 2 PI and the lowest on Day 9 PI. On Day 28 PI, the number of sIg+ cells was still greater than the number of Thy-1.2+ cells. The granulomatous lesions were observed in the liver as early as Day 2 PI and their frequency was maximal on Day 9 PI. Immunohistochemical analysis of the granulomatous lesions showed that macrophages (F4/80+, Mac1+) were the basic cells and that L3T4+ cells were the predominant T cells. In well-developed granulomas observed on Day 9 PI, macrophages were in the centre whereas L3T4+ T cells were preferentially located at the periphery. T cells expressing Lyt-2 antigen were rarely detected. Variations in the proportion of lymphoid cells in the spleen and in hepatic granulomatous lesions suggest different and complementary effector mechanisms in induced immunity against SAO.