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

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 (Ity') 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<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&lt0.05), 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-l.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⁺, Macl⁺) 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. [ABSTRACT FROM AUTHOR]