Salmonella ability to use B-lymphocytes as a reservoir is due to overcoming bactericidal mechanisms, in addition to inability to produce inflammatory cytokines
Abstract number: 1733_308
Rosales-Reyes R., Pérez-López A., Ramírez-Aguilar M., Ortiz-Navarrete V., Urbán-Reyes M., Alpuche-Aranda C.
The ability of Salmonella to survive and replicate within macrophages and dendritic cells is a relevant pathogenic factor to develop disseminated disease. It has also been shown that Salmonella is able to infect B cells in vitro and in vivo. In the mouse model, Salmonella is localised inside B cells (CD19+, B220+) and macrophages (Mac1+) of spleen and bone marrow after 60 days of initial infection.
Objectives: To identify B-Lymphocytes ability to produce bactericidal mechanisms and inflammatory cytokines profile against Salmonella infection.
Methods: Intracellular Salmonella were detected by FACS and UFCs. The nitrogen intermediates reactive (NIR) were quantified by Griess method. The cytotoxicity (ctx) was assay by LDH quantification. TNF-a and IL-1b were detected by ELISA.
Results: The efficiency of Salmonella uptake by B cells increased 10 times when the bacterium was opsonised with specific IgG anti-Salmonella Ab. In addition, the intracellular bacteria were not ctx on infected B cells (even MOI of 1:50) as macrophages (10% vs 38% respectability). Salmonella survives more efficiently in B cells than macrophages at 24 hours post-infection. On the other hand, these Salmonella infected B cells were able to produce NIRs (14.05±3.61 microM without infection, 29.33±3.33 microM with MOI = 50, 75.72±1.39 microM with MOI = 100) in response to magnitude of infection as macrophages (9.33±1.67 microM without infection, 89.33±1.11 microM with MOI = 50 and 116.27±1.39 microM with MOI = 100). Infected B cells are not able to produce IL-1b by inflamosome complex as macrophages (non detected vs 20000 pg/mL respectively).
Conclusions:Salmonella internalisation by B cells is favoured by Fc receptor phagocytosis and is able to survive and evade the bactericidal effect of NIRs. The infected B cells are not able to produce inflammatory cytokines by inflamosome complex (such as IL-1beta) involved in recruitment of effectors immune cells. These data suggest that B cells are a ``safe'' intracellular reservoir for Salmonella and perhaps they are also a mechanism of transportation and evading effectors immune cells during in vivo infection.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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