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Title: Organ-specific fate, recruitment, and refilling dynamics of tissue-resident macrophages during blood-stage Malaria
Authors: Lai, Si Min
Sheng, Jianpeng
Gupta, Pravesh
Renia, Laurent
Duan, Kaibo
Zolezzi, Francesca
Karjalainen, Klaus
Newell, Evan W.
Ruedl, Christiane
Keywords: DRNTU::Science::Biological sciences
Tissue-resident Macrophages
Kupffer Cells
Issue Date: 2018
Source: Lai, S. M., Sheng, J., Gupta, P., Renia, L., Duan, K., Zolezzi, F., . . . Ruedl, C. (2018). Organ-specific fate, recruitment, and refilling dynamics of tissue-resident macrophages during blood-stage Malaria. Cell Reports, 25(11), 3099-3109. doi:10.1016/j.celrep.2018.11.059
Series/Report no.: Cell Reports
Abstract: Inflammation-induced disappearance of tissue-resident macrophages represents a key pathogen defense mechanism. Using a model of systemic blood-stage malaria, we studied the dynamics of tissue-resident macrophages in multiple organs to determine how they are depleted and refilled during the course of disease. We show that Plasmodium infection results in a transient loss of embryonically established resident macrophages prior to the parasitemia peak. Fate-mapping analysis reveals that inflammatory monocytes contribute to the repopulation of the emptied niches of splenic red pulp macrophages and hepatic Kupffer cells, while lung alveolar macrophages refill their niche predominantly through self-renewal. Interestingly, the local microenvironment of the spleen and liver can “imprint” the molecular characteristics of fetal-derived macrophages on newly differentiated bone marrow-derived immigrants with remarkably similar gene expression profiles and turnover kinetics. Thus, the mononuclear phagocytic system has developed distinct but effective tissue-specific strategies to replenish emptied niches to guarantee the functional integrity of the system.
ISSN: 2211-1247
DOI: 10.1016/j.celrep.2018.11.059
Rights: © 2018 The Author(s). This is an open access article under the CC BY-NC-ND license (
Fulltext Permission: open
Fulltext Availability: With Fulltext
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