4 years ago

Chronic Brucella infection induces selective and persistent IFN-γ-dependent alterations of marginal zone macrophages in the spleen.

Letesson JJ, Willemart K, Demars A, Khadrawi A, Muraille E, De Trez C, Machelart A
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+ MZ macrophages (MZMs) and the CD169+ 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 B. 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 and is also observed following B. abortus and B. suis infection. Comparison of wild type and deficient mice suggested that MZ macrophage population loss is dependent on IFN-γR but independent of T cells or TNFαR1 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.

Publisher URL: https://www.ncbi.nlm.nih.gov/pubmed/28808159

DOI: PubMed:28808159

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