Lipopolysaccharide-initiated persistent rhinitis causes gliosis and synaptic loss in the olfactory bulb

Sanae Hasegawa-Ishii, Atsuyoshi Shimada, Fumiaki Imamura

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The olfactory mucosa (OM) is exposed to environmental agents and therefore vulnerable to inflammation. To examine the effects of environmental toxin-initiated OM inflammation on the olfactory bulb (OB), we induced persistent rhinitis in mice and analyzed the spatial and temporal patterns of histopathological changes in the OM and OB. Mice received unilateral intranasal administration of lipopolysaccharide (LPS) or saline three times per week, and were immunohistologically analyzed at 1, 3, 7, 14 and 21 days after the first administration. LPS administration induced an inflammatory response in the OM, including the infiltration of Ly-6G-, CD11b-, Iba-1- A nd CD3-positive cells, the production of interleukin-1β by CD11b- A nd Iba-1-positive cells, and loss of olfactory sensory neurons (OSNs). In the OB, we observed activation of microglia and astrocytes and decreased expression of tyrosine hydroxylase in periglomerular cells, vesicular glutamate transporter 1, a presynaptic protein, in mitral and tufted projection neurons, and 5T4 in granule cells. Thus, the OM inflammation exerted a detrimental effect, not only on OSNs, but also on OB neurons, which might lead to neurodegeneration.

Original languageEnglish (US)
Article number11605
JournalScientific reports
Volume7
Issue number1
DOIs
StatePublished - Dec 1 2017

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Olfactory Mucosa
Gliosis
Olfactory Bulb
Rhinitis
Lipopolysaccharides
Olfactory Receptor Neurons
Inflammation
Vesicular Glutamate Transport Protein 1
Neurons
Intranasal Administration
Tyrosine 3-Monooxygenase
Microglia
Interleukin-1
Astrocytes
Proteins

All Science Journal Classification (ASJC) codes

  • General

Cite this

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abstract = "The olfactory mucosa (OM) is exposed to environmental agents and therefore vulnerable to inflammation. To examine the effects of environmental toxin-initiated OM inflammation on the olfactory bulb (OB), we induced persistent rhinitis in mice and analyzed the spatial and temporal patterns of histopathological changes in the OM and OB. Mice received unilateral intranasal administration of lipopolysaccharide (LPS) or saline three times per week, and were immunohistologically analyzed at 1, 3, 7, 14 and 21 days after the first administration. LPS administration induced an inflammatory response in the OM, including the infiltration of Ly-6G-, CD11b-, Iba-1- A nd CD3-positive cells, the production of interleukin-1β by CD11b- A nd Iba-1-positive cells, and loss of olfactory sensory neurons (OSNs). In the OB, we observed activation of microglia and astrocytes and decreased expression of tyrosine hydroxylase in periglomerular cells, vesicular glutamate transporter 1, a presynaptic protein, in mitral and tufted projection neurons, and 5T4 in granule cells. Thus, the OM inflammation exerted a detrimental effect, not only on OSNs, but also on OB neurons, which might lead to neurodegeneration.",
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Lipopolysaccharide-initiated persistent rhinitis causes gliosis and synaptic loss in the olfactory bulb. / Hasegawa-Ishii, Sanae; Shimada, Atsuyoshi; Imamura, Fumiaki.

In: Scientific reports, Vol. 7, No. 1, 11605, 01.12.2017.

Research output: Contribution to journalArticle

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