Introduction
Chronic rhinosinusitis with nasal polyps(CRSwNP)is a common and frequent disease in otolaryngology. At present, CRSwNP has poor therapeutic and high recurrence rate, and its pathogenesis is not clear. Based on European Position Paper on Rhinosinusitis and Nasal Polyps 2012(EPOS2012)1, The treatment of CRSwNP is mainly represented by nasal corticosteroids combined with nasal endoscopic surgery. Although many patients undergo systematic drug-assisted treatment after surgery, they still had pathological features such as nasal mucosa swelling, vesical and mucus discharge. Symptoms such as nasal obstruction, running nose and distention pain persisted or even got worsen. As the research hotspot in the field of nosology, the pathogenesis and recurrence after surgery have attracted much attention2-4.
At present, most of the studies on CRSwNP focus on the infiltration of inflammatory cells and expression of cytokine in tissues, but there is still little research on the pathologic changes related to edema and degeneration of nasal mucosal cells in patients with CRSwNP. In recent years, journals such as “Nature” , “Cell” and other magazines had reported eukaryotic cells ribosomal pathway and control system of endoplasmic reticulum-associated protein could regulate polypeptide in cells, and then regulate cellular homeostasis5-8. It proved that the mechanism of cell edema induced by hypoxia, infection and other factors was closely related to the changes of mitochondrial function. And the factors mentioned above disrupt the metabolism of protein peptides in cells, which in turn leads to cell edema.
Understanding the pathological changes of nasal polyp clearly is important for further studing the pathogenesis of nasal polyp. The pathological changes of tissue cell edema and remodeling in CRSwNP are characterized by intracellular accumulation of abundant collagen and matrix proteins. A large number of inflammatory cytokines are secreted and promote the remodeling of collagen and matrix proteins in the tissues in CRSwNP. Science reported that accumulation of CLCs proteins reshaped airway mucosa and aggravated airway inflammation9. Thus it can be seen that accumulation of proteins plays an important role in edema of cells in CRSwNP. Effectively removing the accumulation of proteins in CRSwNP tissues may be a very effective treatment for CRSwNP. Therefore, we designed an experiment to study the differential expression of CRSwNP transcriptome genes in tissues with different degrees of edema treated with glucocorticoids, and predicted the possible mechanism.