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IL-33 receptor ST2 regulates the cognitive impairments associated with experimental cerebral malaria. | LitMetric

AI Article Synopsis

  • - Cerebral malaria (CM) has a high mortality rate and can cause long-term cognitive issues in survivors, with a murine model showing similar effects from Plasmodium berghei ANKA (PbA) infection.
  • - Research indicates that PbA infection leads to early memory issues in wild-type mice before any blood-brain barrier damage occurs, while mice lacking the ST2 receptor do not experience these cognitive defects.
  • - The study reveals that PbA infection significantly raises IL-33 levels in the brain, with a feedback loop between IL-1β and IL-33 driving inflammation and neurological problems, particularly through the interaction of microglia and oligodendrocytes.

Article Abstract

Cerebral malaria (CM) is associated with a high mortality rate and long-term neurocognitive impairment in survivors. The murine model of experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (PbA)-infection reproduces several of these features. We reported recently increased levels of IL-33 protein in brain undergoing ECM and the involvement of IL-33/ST2 pathway in ECM development. Here we show that PbA-infection induced early short term and spatial memory defects, prior to blood brain barrier (BBB) disruption, in wild-type mice, while ST2-deficient mice did not develop cognitive defects. PbA-induced neuroinflammation was reduced in ST2-deficient mice with low Ifng, Tnfa, Il1b, Il6, CXCL9, CXCL10 and Cd8a expression, associated with an absence of neurogenesis defects in hippocampus. PbA-infection triggered a dramatic increase of IL-33 expression by oligodendrocytes, through ST2 pathway. In vitro, IL-33/ST2 pathway induced microglia expression of IL-1β which in turn stimulated IL-33 expression by oligodendrocytes. These results highlight the IL-33/ST2 pathway ability to orchestrate microglia and oligodendrocytes responses at an early stage of PbA-infection, with an amplification loop between IL-1β and IL-33, responsible for an exacerbated neuroinflammation context and associated neurological and cognitive defects.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407765PMC
http://dx.doi.org/10.1371/journal.ppat.1006322DOI Listing

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