Distribution Change of Mast Cells in Human Nasal Polyps

Abstract

Recent studies have shown that mast cells are involved in pathophysiologic processes of chronic inflammation. However, little is known about the distribution of mast cells in nasal polyps, which is a chronic inflammatory disease of the upper airways. Biopsy specimens from patients with nasal polyps (n ¼ 20) and control patients without nasal polyps (n ¼ 8) were included in this study. The distribution of mast cells in nasal polyps was determined by immunohistochemistry. Meanwhile, we detected the expression of chemokines (CCL5, CCL11, CX3CL1, IL-8, IL-6) in the epithelial cells of normal nasal mucosa and nasal polyps. In addition, the expression of these chemokines was investigated by western bolting in airway epithelial cells line (A549 cells) under inflammatory condition. Mast cells migrated toward intraepithelium in nasal polyps and the expression of chemokines (CCL5, CCL11, CX3CL1, IL-8) was up-regulated in the epithelial cells of nasal polyps compared with normal nasal mucosa. The expression of chemokines was also up-regulated in A549 cells after Lipopolysaccharide (LPS)-treatment for 3 hr and 6 hr. Our findings showed that mast cells migrate toward intraepithelium in nasal polyps and the overexpression of chemokines (CCL5, CCL11, CX3CL1, IL-8) suggested that they might be responsible for mast cells migration. It implies that mast cell play potential roles in the development of nasal polyps.

Dexpramipexole depletes blood and tissue eosinophils in nasal polyps with no change in polyp size

“…The overrepresentation of mast cells and mast cell mediators within nasal polyps is well described, although the exact clinical consequences driven by the presence of mast cell are not fully understood . In our study, the unexpected qualitative finding of increased numbers of mast cells within the nasal polyp biopsies following treatment with dexpramipexole warrants further mechanistic investigation.…”

“…The overrepresentation of mast cells and mast cell mediators within nasal polyps is well described, although the exact clinical consequences driven by the presence of mast cell are not fully understood. [19][20][21][22] In our study, the unexpected qualitative finding of increased numbers of mast cells within the nasal polyp biopsies following treatment with dexpramipexole warrants further mechanistic investigation. It is not clear whether this finding represents a direct mast cell-enhancing drug effect of dexpramipexole or simply a histological consequence in which the absence of eosinophils allowed for a proportional increase in the numbers of mast cells that can be visualized in each HPF.…”

Hypoxia regulates human mast cell adhesion to fibronectin via the PI3K/AKT signaling pathway

“…This regulation might be an important cellular mechanism determining mast cell distribution in tissues. There are multiple observations of an increased number of mast cells in certain diseased tissues, such as airways of patients with asthma and COPD [39][40][41][42], nasal polyps [43], inflamed periodontal area [44], and stroma of solid tumors [45], possibly due to increased mast cell migration [43,46]. Upregulation of integrin-mediated mast cell adhesion by hypoxia could provide a mechanism for retaining mast cells in areas of inflammatory reaction.…”