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.