Figure 1
Figure 1. Key hematopoietic differences in local versus systemic bacterial infection. Local bacterial infection leads to activation of resident hematopoietic cells (eg, macrophages) as well as nonhematopoietic cells (eg, parenchymal, vascular, or stromal cells), and to subsequent release of inflammatory cytokines and chemokines. As a net result, myeloid effector cells are attracted to the site of infection, where they exert their antimicrobial functions under the influence of locally produced cytokines. Apart from local signs of infection (calor, dolor, rubor, tumor, and functio laesa), no systemic effects such as peripheral blood leukocytosis or left-shift are induced (left). By contrast, locally noncontrolled infection (eg, sepsis) leads to systemic symptoms such as fever, peripheral blood leukocytosis, and left-shift. Concomitantly, BM myelopoiesis is massively enhanced above steady-state levels (emergency myelopoiesis) to provide myeloid effector cells needed to resolve the infection (right).

Key hematopoietic differences in local versus systemic bacterial infection. Local bacterial infection leads to activation of resident hematopoietic cells (eg, macrophages) as well as nonhematopoietic cells (eg, parenchymal, vascular, or stromal cells), and to subsequent release of inflammatory cytokines and chemokines. As a net result, myeloid effector cells are attracted to the site of infection, where they exert their antimicrobial functions under the influence of locally produced cytokines. Apart from local signs of infection (calor, dolor, rubor, tumor, and functio laesa), no systemic effects such as peripheral blood leukocytosis or left-shift are induced (left). By contrast, locally noncontrolled infection (eg, sepsis) leads to systemic symptoms such as fever, peripheral blood leukocytosis, and left-shift. Concomitantly, BM myelopoiesis is massively enhanced above steady-state levels (emergency myelopoiesis) to provide myeloid effector cells needed to resolve the infection (right).

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