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in Mice in Response to Acute Pneumovirus Infection Cells Driven by Proinflammatory Cytokines Production and Differentiation of Myeloid

Respiratory virus infections are often pathogenic, driving severe inﬂammatory responses. Most research has focused on localized effects of virus infection and inﬂammation. However, infection can induce broad-reaching, systemic changes that are only beginning to be characterized. In this study, we assessed the impact of acute pneumovirus infection in C57BL/6 mice on bone marrow hematopoiesis. We hypothesized that inﬂammatory cytokine production in the lung upregulates myeloid cell production in response to infection. We demonstrate a dramatic increase in the percentages of circulating myeloid cells, which is associated with pro-nounced elevations in inﬂammatory cytokines in serum (IFN- g , IL-6, CCL2), bone (TNF- a ), and lung tissue (TNF- a , IFN- g , IL-6, CCL2, CCL3, G-CSF, osteopontin). Increased hematopoietic stem/progenitor cell percentages (Lineage 2 Sca-I + c-kit + ) were also detected in the bone marrow. This increase was accompanied by an increase in the proportions of committed myeloid progenitors, as determined by colony-forming unit assays. However, no functional changes in hematopoietic stem cells occurred, as assessed by competitive bone marrow reconstitution. Systemic administration of neutralizing Abs to either TNF- a or IFN- g blocked expansion of myeloid progenitors in the bone marrow and also limited virus clearance from the lung. These ﬁndings suggest that acute inﬂammatory cytokines drive production and differentiation of myeloid cells in the bone marrow by inducing differentiation of committed myeloid progenitors.