HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: jimmunol.0900612v1 183/3/1900    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Serbina, N. V. Articles by Pamer, E. G. PubMed PubMed Citation Articles by Serbina, N. V. Articles by Pamer, E. G.

Selective Expansion of the Monocytic Lineage Directed by Bacterial Infection¹

Infectious Disease Service, Department of Medicine, Memorial Sloan-Kettering Cancer Center, Immunology Program, Sloan-Kettering Institute, New York, NY 10021

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 costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ The authors’ research is supported by the National Institutes of Health (Grants R37 AI39031 and P01 CA023766-30 to E.G.P; K12 CA120121 to N.V.S.; and K08 AI071998 to T.M.H.) and Irvington Institute for Immunological Research (to N.V.S.).

N.V.S. conceived, designed, and performed research, analyzed data, and wrote the paper; T.M.H. generated CCR2 reporter mice; M.C. performed research; and E.G.P. designed research and wrote the paper.

² N.V.S. and T.M.H. contributed equally.

³ Address correspondence and reprint requests Dr. Natalya V. Serbina, Infectious Diseases Service, Memorial Sloan-Kettering Cancer Center, Sloan Kettering Institute, 1275 York Avenue, New York, NY 10021. E-mail address: serbinan{at}mskcc.org

⁴ Abbreviations used in this paper: iNOS, inducible NO synthase; MDP, macrophage and dendritic cell progenitor; BAC, bacterial artificial chromosome; miRNA, microRNA; ICE, IL-1β-converting enzyme.