4.4 Article

Immune cell infiltration and related core genes expression characteristics in eosinophilic and non-eosinophilic chronic rhinosinusitis with nasal polyps

Journal

EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 20, Issue 6, Pages -

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2020.9310

Keywords

immune cell infiltration; eosinophilic chronic rhinosinusitis with nasal polyps; non-eosinophilic chronic rhinosinusitis with nasal polyps; gene expression; differential analysis

Funding

  1. National Natural Science Foundation of China [81673809]
  2. Scientific and Technological Program of Zhejiang province [2017F10024]
  3. Traditional Chinese Medicine Scientific Program of Zhejiang province [2016ZQ002]
  4. National Natural Science Foundation of Zhejiang province [LY19H280005]
  5. Medical and health Scientific and Technological Program of Zhejiang province [2019KY347]

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Chronic rhinosinusitis with nasal polyps (CRSwNP) refers to chronic inflammation of the sinonasal mucosa. It can either be eosinophilic (ECRSwNP) or non-eosinophilic (non-ECRSwNP). However, immune cell infiltration in the microenvironment and pathogenesis of ECRSwNP and non-ECRSwNP are still unclear. The aim of the present study was to assess the immune cell infiltration and molecular mechanisms of ECRSwNP and non-ECRSwNP. In the present study, 22 immune cell types in ECRSwNP and non-ECRSwNP were investigated by CIBERSORT based on transcriptome data. The core gene related pathophysiology of CRSwNP was analyzed using Weighted Gene Correlation Network Analysis according to the phenotype of the infiltrated eosinophils and nasal polyps (NP). A total of four types of immune cells (mast cells, activated dendritic cells, M2 macrophages and activated natural killer cells) were demonstrated to have a direct and indirect correlation with eosinophilic infiltration in ECRSwNP. M1 macrophages and activated CD4(+) memory T cells were correlated with major immune cell types in non-ECRSwNP. NP could affect the expression of 'olfactory receptor activity' and 'channel activity' genes to impair the olfactory signaling pathway and neuroactive ligand receptor pathway. 'Cell adhesion molecule binding', 'cytokine receptor binding' and 'glucocorticoid receptor binding' were significantly enriched in ECRSwNP, whereas epithelial cell injury, autophagy and the mTOR pathway (hsa04140 and hsa04150) may serve an important role in the pathogenesis of non-ECRSwNP. There were significantly different immune cell infiltration and related core genes expression characteristics between ECRSwNP and non-ECRSwNP. The results of the present study provide an improved basis for elucidation of the mechanism and treatment of CRSwNP.

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