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Olfactory plays a key role in spatiotemporal pathogenesis of cerebral malaria

Hong Zhao1, Taiki Aoshi2, Satoru Kawai3

  • 1Laboratory of Malaria Immunology, Immunology Frontier Research Center (IFReC), Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.

Cell Host & Microbe
|May 17, 2014
PubMed

Insights

Cerebral malaria damages the olfactory bulb, causing loss of smell. Blocking specific cell recruitment pathways may offer new therapeutic strategies for this severe complication of Plasmodium falciparum infection.

Area of Science:

  • Neuroscience
  • Immunology
  • Infectious Diseases

Background:

  • Cerebral malaria (CM) is a severe Plasmodium falciparum complication with poorly understood neuroinflammatory mechanisms.
  • Experimental cerebral malaria (ECM) models suggest blood-brain barrier disruption and CD8 T cell infiltration are key factors.

Purpose of the Study:

  • To investigate the spatiotemporal mechanisms of brain damage in ECM.
  • To identify specific pathological pathways in the olfactory bulb during ECM.

Main Methods:

  • Ultra-high-field MRI and multiphoton microscopy were used in a mouse model of ECM.
  • Analysis of chemokine and receptor expression (CCL21, CCR7, CXCR3) and CD8 T cell responses.

Main Results:

  • Plasmodium parasites physically and functionally damage the olfactory bulb in ECM, leading to smell loss.
  • Parasite accumulation, cell occlusion, and microbleeding occur in olfactory bulb capillaries, correlating with fever and cytokine storm.
  • Upregulation of CCL21 in the olfactory bulb and blockade of CCR7/CXCR3 reduced CD8 T cell activation and improved survival.

Conclusions:

  • The olfactory bulb is a vulnerable site for damage during experimental cerebral malaria.
  • Olfaction loss can be an early indicator of ECM.
  • Targeting CCL21/CCR7/CXCR3 pathways may represent a novel therapeutic strategy for cerebral malaria.

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