Distinct gene expression profiles and regulation networks of nasal polyps in eosinophilic and non-eosinophilic chronic rhinosinusitis

2018 ◽  
Vol 8 (5) ◽  
pp. 592-604 ◽  
Author(s):  
Naoko Okada ◽  
Tsuguhisa Nakayama ◽  
Daiya Asaka ◽  
Natsuki Inoue ◽  
Tadao Tsurumoto ◽  
...  
2021 ◽  
Author(s):  
Ayaka Nakatani ◽  
Takeshi Tsuda ◽  
Yohei Maeda ◽  
Masaki Hayama ◽  
Daisuke Okuzaki ◽  
...  

Abstract Chronic rhinosinusitis is classified into eosinophilic chronic rhinosinusitis (ECRS) and non-eosinophilic chronic rhinosinusitis (NECRS). ECRS is a refractory allergic disease involving a variety of immune and epithelial cells. S100A8 is a damage-associated molecular pattern that is closely related to allergic inflammation. However, the pathological implications of S100A8 in ECRS have not been clarified. We evaluated the role of S100A8 in the pathogenesis of ECRS. Gene expression profiles of nasal polyps obtained from patients with ECRS or NECRS were evaluated using RNA sequencing. S100A8 was identified as a significantly upregulated gene in nasal polyps associated with ECRS. Immunohistochemistry consistently revealed intense S100A8 staining in nasal polyps from patients with ECRS. Human nasal epithelial cells expressed the receptor for advanced glycation end products and Toll-like receptor 4. Recombinant S100A8 protein induced interleukin-1β secretion in human nasal epithelial cells. Our data demonstrate that S100A8 results in production of interleukin-1β in the nasal epithelium, which may be involved in the pathogenesis of ECRS.


Oncogene ◽  
2002 ◽  
Vol 21 (18) ◽  
pp. 2926-2937 ◽  
Author(s):  
Oona Delpuech ◽  
Jean-Baptiste Trabut ◽  
Françoise Carnot ◽  
Jean Feuillard ◽  
Christian Brechot ◽  
...  

2020 ◽  
Vol 318 (4) ◽  
pp. L684-L697 ◽  
Author(s):  
Valentina Biasin ◽  
Slaven Crnkovic ◽  
Anita Sahu-Osen ◽  
Anna Birnhuber ◽  
Elie El Agha ◽  
...  

Pulmonary fibrosis is characterized by pronounced collagen deposition and myofibroblast expansion, whose origin and plasticity remain elusive. We utilized a fate-mapping approach to investigate α-smooth muscle actin (αSMA)+ and platelet-derived growth factor receptor α (PDGFRα)+ cells in two lung fibrosis models, complemented by cell type-specific next-generation sequencing and investigations on human lungs. Our data revealed that αSMA+ and PDGFRα+ cells mark two distinct mesenchymal lineages with minimal transdifferentiation potential during lung fibrotic remodeling. Parenchymal and perivascular fibrotic regions were populated predominantly with PDGFRα+ cells expressing collagen, while αSMA+ cells in the parenchyma and vessel wall showed variable expression of collagen and the contractile protein desmin. The distinct gene expression profile found in normal conditions was retained during pathologic remodeling. Cumulatively, our findings identify αSMA+ and PDGFRα+ cells as two separate lineages with distinct gene expression profiles in adult lungs. This cellular heterogeneity suggests that anti-fibrotic therapy should target diverse cell populations.


Oncology ◽  
2008 ◽  
Vol 75 (1-2) ◽  
pp. 71-80 ◽  
Author(s):  
Zeenath Jehan ◽  
Abdul K. Siraj ◽  
Jehad Abubaker ◽  
Christian Ruiz ◽  
Ronald Simon ◽  
...  

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