ArticleJournal of neuroinflammation2026
CCL5 and CD11b-fibrin interactions regulate microglia migration and morphology in hyperinflammatory experimental cerebral malaria.
Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMicrogliosis and severe coagulation, including fibrinogen deposition, are features of both experimental and human cerebral malaria (CM), a lethal disease. Vascular-associated microglia migrate to coagulated cerebral vessels containing inflammatory monocytes and T cells in experimental CM. We previously showed that microglial depletion exacerbates coagulation and disease severity, including hypothermia, while anticoagulant treatment reduces microgliosis and prevents mortality. These data suggest an overall protective effect of microglia on eCM, and indicate a link between microgliosis, hypothermia, and coagulation. Therefore, mechanisms of migration and activation of microglia, T cells, and monocytes were studied in relation to the role of fibrin(ogen) in eCM.
methodsUsing both Plasmodium berghei ANKA infection or experimental CM, and P. chabaudi infection of IL-10-deficient mice (IL-10 KO), which causes a hyperinflammatory response including neuropathology, intravital two-photon microscopy and flow cytometry, were used to test patterns and mechanisms of migration. In vivo methods included intranasal administration of CCL5 receptor antagonist Met-CCL5; systemic integrin-blocking antibodies and mutant animals (IL-10 KO, ICAM1 KO), and anticoagulant treatment. Clotting-deficient mice (Fga KO, Fib
resultsIntraluminal adhesion and crawling of CCR2
conclusionsThese data support our previous study suggesting that microglia are involved in the regulation of hypothermia in eCM and reveal CCL5 and fibrin-CD11b signaling in microglia as key molecular pathways modulating neuroinflammation in malaria.
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