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Systemic Salmonella infection commonly induces prolonged splenomegaly in murine or human hosts. Although this increase in splenic cellularity is often assumed to be due to the recruitment and expansion of leukocytes, the actual cause of splenomegaly remains unclear. We monitored spleen cell populations during Salmonella infection and found that the most prominent increase is found in the erythroid compartment. At the peak of infection, the majority of spleen cells are immature CD71−Ter119+ reticulocytes, indicating that massive erythropoiesis occurs in response to Salmonella infection. Indeed, this increase in RBC precursors corresponded with marked elevation of serum erythropoietin (EPO). Furthermore, the increase in RBC precursors and EPO production required innate immune signaling mediated by Myd88/TRIF. Neutralization of EPO substantially reduced the immature RBC population in the spleen and allowed a modest increase in host control of infection. These data indicate that early innate immunity to Salmonella initiates marked splenic erythropoiesis and may hinder bacterial clearance.

Acknowledgements: These studies were supported by funding from the British Heart

Early experience with the GORE Acuseal is encouraging. Patency and bacteremia rates are at least comparable to standard polytetrafluoroethylene grafts. ecAVGs have permitted cannulation within 24 hours of insertion and line avoidance in the majority of patients. Nearly three-quarters of patients achieved a definitive "personal vascular access solution" from their ecAVG.

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