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Excessive Expression of Microglia/Macrophage and Proinflammatory Mediators in Olfactory Bulb and Olfactory

Chien-Fu Yeh1,2,3, Tung-Yueh Chuang4, Ming-Ying Lan1,2

  • 1Department of Otolaryngology-Head and Neck Surgery, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C.

In Vivo (Athens, Greece)
|October 31, 2019
PubMed
Abstract

Insights

Ischemic stroke impairs sense of smell by activating brain immune cells. This neuroinflammation in the olfactory bulb reduces olfactory marker protein (OMP) levels, leading to olfactory dysfunction.

Area of Science:

  • Neuroscience
  • Immunology
  • Stroke Research

Background:

  • Olfactory dysfunction is a known consequence of stroke, but its underlying mechanisms remain incompletely understood.
  • Microglia activation in the olfactory bulb is implicated in olfactory dysfunction.
  • Middle cerebral artery occlusion (MCAO) models suggest ipsilateral olfactory bulb microglia activation post-stroke.

Purpose of the Study:

  • To investigate the pathogenesis of olfactory dysfunction following ischemic stroke.
  • To explore the role of microglia activation and neuroinflammation in the olfactory bulb after MCAO.

Main Methods:

  • A rat model of middle cerebral artery occlusion (MCAO) was employed to simulate ischemic stroke.
  • Olfactory function was assessed using the buried food test.
  • mRNA expression of olfactory marker protein (OMP), microglia/macrophage activation markers, and proinflammatory mediators was quantified via RT-qPCR.

Main Results:

  • Rats subjected to MCAO exhibited significantly impaired olfactory performance.
  • A decrease in olfactory marker protein (OMP) mRNA expression was observed in the olfactory bulb.
  • Increased mRNA expression of microglia/macrophage activation and proinflammatory mediators was detected in the olfactory bulb.

Conclusions:

  • Ischemic stroke induces microglia/macrophage activation and promotes neuroinflammation within the olfactory bulb.
  • This inflammatory response in the olfactory bulb is a key factor contributing to stroke-induced olfactory dysfunction.
Keywords:
Olfactory dysfunctionischemic strokemacrophagemicrogliamiddle cerebral artery occlusionproinflammatory mediatorrat

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