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Chronic Brucella Infection Induces Selective and Persistent Interferon Gamma-Dependent Alterations of Marginal Zone Macrophages in the Spleen.
- Source :
-
Infection and immunity [Infect Immun] 2017 Oct 18; Vol. 85 (11). Date of Electronic Publication: 2017 Oct 18 (Print Publication: 2017). - Publication Year :
- 2017
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Abstract
- The spleen is known as an important filter for blood-borne pathogens that are trapped by specialized macrophages in the marginal zone (MZ): the CD209 <superscript>+</superscript> MZ macrophages (MZMs) and the CD169 <superscript>+</superscript> marginal metallophilic macrophages (MMMs). Acute systemic infection strongly impacts MZ populations and the location of T and B lymphocytes. This phenomenon has been linked to reduced chemokine secretion by stromal cells. Brucella spp. are the causative agent of brucellosis, a widespread zoonotic disease. Here, we used Brucella melitensis infection as a model to investigate the impact of chronic stealth infection on splenic MZ macrophage populations. During the late phase of Brucella infection, we observed a loss of both MZMs and MMMs, with a durable disappearance of MZMs, leading to a reduction of the ability of the spleen to take up soluble antigens, beads, and unrelated bacteria. This effect appears to be selective as every other lymphoid and myeloid population analyzed increased during infection, which was also observed following Brucella abortus and Brucella suis infection. Comparison of wild-type and deficient mice suggested that MZ macrophage population loss is dependent on interferon gamma (IFN-γ) receptor but independent of T cells or tumor necrosis factor alpha receptor 1 (TNF-αR1) signaling pathways and is not correlated to an alteration of CCL19, CCL21, and CXCL13 chemokine mRNA expression. Our results suggest that MZ macrophage populations are particularly sensitive to persistent low-level IFN-γ-mediated inflammation and that Brucella infection could reduce the ability of the spleen to perform certain MZM- and MMM-dependent tasks, such as antigen delivery to lymphocytes and control of systemic infection.<br /> (Copyright © 2017 American Society for Microbiology.)
- Subjects :
- Animals
Anti-Bacterial Agents pharmacology
B-Lymphocytes immunology
B-Lymphocytes microbiology
Brucella abortus drug effects
Brucella abortus immunology
Brucella abortus pathogenicity
Brucella melitensis drug effects
Brucella melitensis immunology
Brucella melitensis pathogenicity
Brucella suis drug effects
Brucella suis immunology
Brucella suis pathogenicity
Brucellosis drug therapy
Brucellosis genetics
Brucellosis microbiology
Chemokine CCL19 genetics
Chemokine CCL19 immunology
Chemokine CCL21 genetics
Chemokine CCL21 immunology
Chemokine CXCL13 genetics
Chemokine CXCL13 immunology
Chronic Disease
Gene Expression Regulation
Interferon-gamma genetics
Macrophages microbiology
Mice
Mice, Inbred C57BL
Mice, Knockout
RNA, Messenger genetics
RNA, Messenger immunology
Receptors, Interferon deficiency
Receptors, Interferon genetics
Receptors, Tumor Necrosis Factor, Type I deficiency
Receptors, Tumor Necrosis Factor, Type I genetics
Receptors, Tumor Necrosis Factor, Type I immunology
Rifampin pharmacology
Signal Transduction
Spleen microbiology
Streptomycin pharmacology
T-Lymphocytes immunology
T-Lymphocytes microbiology
Interferon gamma Receptor
Brucellosis immunology
Host-Pathogen Interactions
Interferon-gamma immunology
Macrophages immunology
Receptors, Interferon immunology
Spleen immunology
Subjects
Details
- Language :
- English
- ISSN :
- 1098-5522
- Volume :
- 85
- Issue :
- 11
- Database :
- MEDLINE
- Journal :
- Infection and immunity
- Publication Type :
- Academic Journal
- Accession number :
- 28808159
- Full Text :
- https://doi.org/10.1128/IAI.00115-17