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. Author manuscript; available in PMC: 2011 Jul 18.
Published in final edited form as: J Immunol. 2010 Oct 15;185(10):6198–6204. doi: 10.4049/jimmunol.1001198

FIGURE 6.

FIGURE 6

Salmonella infection-induced EPO production and erythroid expansion is dependent on Myd88/TRIF expression. A, C57BL/6 mice were infected i.v. with 5 × 105 attenuated Salmonella, BRD509, and blood was collected at weekly intervals. EPO concentrations were measured at weekly time points. The graph shows the mean serum EPO ± SD for three to five mice per time point and is representative of three individual experiments. B–D, C57BL/6 WT and Myd88/TRIF-deficient mice were infected i.v. with 5 × 105 attenuated Salmonella. Spleens and/or peripheral blood were harvested at weekly time points. EPO concentrations were measured in blood (B), bacterial CFUs were determined (C), and splenic erythroid cell populations were examined by flow cytometry (D). B, The graph shows the mean serum EPO ± SD for three to five mice per time point and is representative of two individual experiments. The mean EPO concentration was significantly lower in the blood of Salmonella-infected Myd88/TRIF-deficient mice at days 4 and 8. C, The graph shows bacterial CFUs at day 8 postinfection and is representative of two individual experiments. The mean bacterial counts were significantly higher in Myd88/TRIF-deficient mice. D, The graphs show mean percentage and total number of Ter119+/CD71+ cells in the spleen ± SD for three to five mice per group and are representative of two individual experiments. The mean percentage and total number of Ter119+/CD71+ cells was significantly lower in Salmonella-infected Myd88/TRIF-deficient mice. *p < 0.05, as determined by Student t test.