Stimulation of erythropoiesis in mice with mycoplasma infection

Investigating the role of bone marrow stroma in the response of haematopoietic stem cells to plasmodium berghei infection

“…Both murine and human HSCs express Toll-like receptors (TLRs) (Kim et al, 2005;Nagai et al, 2006;Sioud et al, 2006;Sioud & Fløisand, 2007), suggesting the presence of an early sensing mechanism for HSCs to detect infection and respond with the immediate production of immune effector cells. Previous work has demonstrated that TLR signalling is necessary for the HSC response to systemic infection (Rodriguez et al, 2009) and that LPS can directly stimulate HSCs in vivo to induce increased cycling (Kaulen et al, 1983;Takizawa et al, 2017) and mobilization out of the BM (Ueda et al, 2004). It has also been proposed that HSPCs possess immunosurveillance properties and a subset are continuously surveying extramedullary non-lymphoid tissues (Massberg et al, 2007).…”

“…Upon infection, this number significantly increases to ensure sufficient production of the mature cells required to combat invading pathogens and it is now widely accepted that this shift in progeny output can be driven by HSCs themselves as they are highly responsive to the inflammatory conditions that exist in the BM during infection and are able to detect pathogens via the expression of pathogen pattern recognition receptors. As discussed in Chapter 1, it is also known that various infections and inflammatory cytokines can drive HSCs out of their quiescent state to induce increased cycling and mobilization out of the BM (Kaulen et al, 1983;Ueda et al, 2004;Rodriguez et al, 2009;Takizawa, Boettcher & Manz, 2012). Reports on how these insults alter the function of HSCs are varied but it is likely that all severe infections, even after they have been cleared, have deleterious effects on these cells in the long-term.…”