Journal
JOURNAL OF IMMUNOLOGY
Volume 183, Issue 3, Pages 1900-1910Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0900612
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Funding
- NCI NIH HHS [K12 CA120121, P01 CA023766, P01 CA023766-310044, P01 CA023766-30] Funding Source: Medline
- NIAID NIH HHS [R37 AI039031, R37 AI039031-14, R37AI39031, R01 AI080619, K08AI071998, K08 AI071998] Funding Source: Medline
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CCR2-mediated recruitment of Ly6C(high) monocytes is essential for defense against a range of microbial pathogens. Although our understanding of monocyte trafficking to inflammatory sites is increasing, how innate immune inflammation influences monocyte development and maturation during microbial infection remains undefined. Herein, we demonstrate that infection with the intracellular bacterial pathogen Listeria monocytogenes specifically and selectively promotes monopoiesis. Systemic infection with virulent L. monocytogenes induces marked proliferation of bone marrow monocyte precursors and results in depletion of myeloid progenitors. Proliferation of monocyte precursors correlates with the intensity of systemic infection and is unaffected by the density of monocytes in the bone marrow. Although MyD88/Trif-mediated signaling is not required for early emigration of the mature monocyte population from the bone marrow, replenishment of monocyte populations depends on MyD88/Trif. Our studies demonstrate that TLR-mediated signals play an essential role in the maintenance of monocyte homeostasis during systemic bacterial infection. The Journal of Immunology, 2009, 183: 1900-1910.
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