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

Yeh, Ching-Fa; Chuang, Tung-Yueh; Lan, Ming‐Ying; Chin, Yu‐Ching; Wang, Wei‐Hsin; Lin, Yung-Yang

doi:10.21873/invivo.11683

Cited by 10 publications

(5 citation statements)

References 20 publications

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“…Multiple stereotyped and time-dependent profiles of gene expression were identified within 24 h. As noted in the study, temporally overlapping profiles have the potential to provide a biological "stroke clock" to stroke prevention [89]. Additionally, mRNA expression of genes for inflammatory Iba-1, CD68, CD16 and CD86 proteins was increased in the ipsilateral olfactory bulb compared to the contralateral side 3 days after tMCAO in rats [90]. Recently, gene expression changes in cells during neuroinflammation were identified 24 h after tMCAO using single cell sequencing (scRNA-Seq).…”

Section: Transcriptomics Of Ismentioning

confidence: 64%

Are Ischemic Stroke and Alzheimer’s Disease Genetically Consecutive Pathologies?

Filippenkov,

Khrunin,

Mozgovoy

et al. 2023

Biomedicines

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Complex diseases that affect the functioning of the central nervous system pose a major problem for modern society. Among these, ischemic stroke (IS) holds a special place as one of the most common causes of disability and mortality worldwide. Furthermore, Alzheimer’s disease (AD) ranks first among neurodegenerative diseases, drastically reducing brain activity and overall life quality and duration. Recent studies have shown that AD and IS share several common risk and pathogenic factors, such as an overlapping genomic architecture and molecular signature. In this review, we will summarize the genomics and RNA biology studies of IS and AD, discussing the interconnected nature of these pathologies. Additionally, we highlight specific genomic points and RNA molecules that can serve as potential tools in predicting the risks of diseases and developing effective therapies in the future.

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Section: Transcriptomics Of Ismentioning

confidence: 64%

Are Ischemic Stroke and Alzheimer’s Disease Genetically Consecutive Pathologies?

Filippenkov,

Khrunin,

Mozgovoy

et al. 2023

Biomedicines

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“…This may imply that resting microglia in the olfactory bulb may be triggered by sinonasal inflammation to transform into activated microglia and then secrete inflammatory mediators. 9 The relative mRNA expression levels of pro-inflammatory mediators including IFN-γ, NOS2, MCP-1, and TNF-α in the olfactory bulb were significantly upregulated, while significant downregulation of OMP and NeuN, of marker post-mitotic neurons, was observed in the LPS group. The protein levels of IFN-γ and TNF-α in the olfactory bulb were also significantly higher in the LPS group.…”

Section: Discussionmentioning

confidence: 89%

“…8 Olfactory impairment develops when neuroinflammation occurs in the olfactory bulb in a rat model of experimental stroke. 9 To date, the number of related rhinosinusitis models has been limited and most studies did not include parameters concerning olfactory function. [10][11][12][13][14][15][16][17] Lipopolysaccharides (LPS), one of the major components of the bacterial endotoxin of Gram-negative bacilli, are able to activate neutrophils to induce an immune response and subsequent sinonasal inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Lipopolysaccharide-Initiated Rhinosinusitis Causes Neuroinflammation and Olfactory Dysfunction in Mice

Yeh

Huang

Lan

et al. 2022

Am J Rhinol�Allergy

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Background Olfactory dysfunction is a common disease and it may be caused by sinonasal inflammation, toxin inhalation, or neurological disorders. After sinonasal inflammation, if both olfactory neuroinflammation and olfactory dysfunction occur still under investigation. Objective This study aimed to investigate whether neuroinflammation and olfactory dysfunction occur after lipopolysaccharide (LPS)-initiated rhinosinusitis. Methods Adult C57BL/6 mice were intranasally administered with LPS for 3 weeks. The olfactory function was evaluated with a buried food test. The inflammatory status of sinonasal cavity and olfactory bulb was evaluated with histology and biochemistry. Results After 3-week LPS treatment, mice developed olfactory dysfunction, sinonasal cavity, and olfactory bulb inflammation. LPS-treated mice had greater sinonasal mucosal thickness. Besides, pro-inflammatory interleukin-6, the number of goblet cells and neutrophils in the sinonasal cavity was increased after LPS administration. The olfactory sensory neurons in the olfactory epithelium and the olfactory bulb were decreased, and the olfactory function was impaired by LPS administration. Inflammatory cytokines such as interferon-γ and tumor necrosis factor-α were increased in the olfactory bulb. Conclusion This study showed that LPS-initiated rhinosinusitis caused olfactory neuroinflammation and olfactory dysfunction in mice.

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“…As Table 1 shows, we observed that the organ coe cient after co-exposure was signi cantly higher than those in the CON group, meaning that there may be pathological injury like brain edema. Then, the buried pellet test, which can evaluate rodents' olfactory function and odor recognition ability, was processed (van Zyl et al, 2016; Lee et al, 2019;Yeh et al, 2019). Olfactory dysfunction can be an essential indicator of learning and memory impairment.…”

Section: Causes Brain Damage In Female Micementioning

confidence: 99%

Combined exposure to high-cholesterol diet and PM 2.5 : Brain injury and regulatory mechanism of HIF-1α in female mice

Chen

Bai

et al. 2023

Preprint

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High-cholesterol diet (HCD) and fine particulate matter (PM2.5) are related to stroke. The comprehensive influence of two factors on stroke is not well known, especially for females. In this study, we investigated brain injury and behavioral changes in female mice exposed to HCD plus PM2.5 for three months and six months, respectively. We measured gene expression of some factors related to stroke and the blood-brain barrier (BBB) in different groups of mice and further explored molecular mechanisms of epigenetic regulation of hypoxia-inducible factor-1α (HIF-1α). The results showed that HCD and PM2.5 co-exposure altered brain-body weight ratio, induced brain pathology damage and behavioral abnormality and elevated inflammatory markers (IL-6 and TNF-α) in mice relative to exposure to PM2.5 or HCD alone. Six-month exposure caused more severe brain damage than that three-month exposure. Co-exposure significantly changed the expressions of HIF-1α and the key genes (VEGF/COX-2/MMP-9/ZO-1/Occludin) in the HIF-1α signaling pathway in the brains of mice compared to the single exposure. Interestingly, HIF-1α was epigenetic regulated by histone deacetylase 4 (HDAC4) and histone 3 lysine 9 acetylation (H3K9ac) by chromatin immunoprecipitation (ChIP) assay. It suggests that the HIF-1α pathway exerts a crucial regulatory role in brain injury and behavioral abnormality in female mice after six-month exposure to HCD plus PM2.5, which are potential mechanisms for HCD and PM2.5-triggering stroke risk in female individuals.

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

Cited by 10 publications

References 20 publications

Are Ischemic Stroke and Alzheimer’s Disease Genetically Consecutive Pathologies?

Are Ischemic Stroke and Alzheimer’s Disease Genetically Consecutive Pathologies?

Lipopolysaccharide-Initiated Rhinosinusitis Causes Neuroinflammation and Olfactory Dysfunction in Mice

Combined exposure to high-cholesterol diet and PM 2.5 : Brain injury and regulatory mechanism of HIF-1α in female mice

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