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Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins
Published on: June 14, 2016
Relation of epidermal growth factor receptor expression to mucus hypersecretion in diffuse panbronchiolitis
Je-Hyeong Kim1, Ki-Hwan Jung, Joung-Ho Han
1Pulmonary Division, Department of Internal Medicine, Korea University Guro Hospital, 97 Gurodong-gil, Guro-gu, Seoul, Korea.
Study Object:
Diffuse panbronchiolitis (DPB) is a hypersecretory airway disease, and the mechanism of mucus hypersecretion in DPB is poorly understood. Moreover, mucin synthesis in the airways has been reported to be regulated by neutrophilic inflammation-induced epidermal growth factor receptor (EGFR) expression, and the degranulation of goblet cells is known to be mediated by neutrophilic elastase. In this study, we examined the relationship between EGFR expression in the bronchiolar epithelium with neutrophilic inflammation and mucus hypersecretion in the tissues of DPB patients.
Design:
The tissue specimens of 13 DPB patients and 6 healthy control subjects were examined by alcian blue/periodic acid-Schiff (AB/PAS) staining for mucous glycoconjugates, and by immunohistochemical staining for MUC5AC, EGFR, tumor necrosis factor-alpha, and CD16 on neutrophils.
Results:
Neutrophilic inflammation was significantly higher in the tissue of DPB patients than in that of control subjects (p = 0.002). In the bronchiolar epithelium, goblet cell metaplasia, by AB/PAS staining and mucin MUC5AC expression, was significantly higher than that in control subjects (p = 0.001 and p = 0.002, respectively). In addition, the morphometric quantification of intraluminal mucus secretion showed that the areas of the bronchiolar lumen occupied by mucus secretion were significantly increased in the tissue of DPB patients (p = 0.001), suggesting goblet cell degranulation. EGFR expression was observed in the bronchiolar epithelium of DPB patients, but not in that of control subjects.
Conclusions:
In DPB, we suggest that mucus hypersecretion due to goblet cell metaplasia is closely associated with neutrophilic inflammation and the expression of EGFR. The study also shows that intraluminal secretion due to the degranulation of goblet cells degranulation is related to neutrophilic inflammation.
Insights
Mucus hypersecretion in diffuse panbronchiolitis (DPB) is linked to neutrophilic inflammation and epidermal growth factor receptor (EGFR) expression. Goblet cell metaplasia and degranulation contribute to increased mucus in DPB airways.
Area of Science:
- Pulmonary Medicine
- Respiratory Diseases
- Pathology
Background:
- Diffuse panbronchiolitis (DPB) is characterized by excessive mucus production, but the underlying mechanisms remain unclear.
- Neutrophilic inflammation and epidermal growth factor receptor (EGFR) signaling are implicated in airway hypersecretory diseases.
- Goblet cell degranulation, a key process in mucus secretion, is influenced by neutrophilic elastase.
Purpose of the Study:
- To investigate the association between EGFR expression, neutrophilic inflammation, and mucus hypersecretion in DPB patients.
- To explore the role of goblet cell metaplasia and degranulation in the pathogenesis of DPB.
Main Methods:
- Tissue samples from 13 DPB patients and 6 healthy controls were analyzed.
- Alcian blue/periodic acid-Schiff (AB/PAS) staining was used to assess mucous glycoconjugates.
- Immunohistochemical staining identified MUC5AC, EGFR, tumor necrosis factor-alpha, and CD16 (neutrophils).
Main Results:
- DPB patients exhibited significantly higher neutrophilic inflammation compared to controls (p = 0.002).
- Goblet cell metaplasia and MUC5AC expression were significantly elevated in DPB bronchiolar epithelium (p = 0.001 and p = 0.002).
- Increased intraluminal mucus secretion, indicative of goblet cell degranulation, was observed in DPB tissues (p = 0.001), with EGFR expression present in the bronchiolar epithelium.
Conclusions:
- Mucus hypersecretion in DPB is closely associated with neutrophilic inflammation and EGFR expression.
- Goblet cell metaplasia and degranulation play significant roles in DPB mucus overproduction.
- Neutrophilic inflammation appears to drive goblet cell degranulation in DPB.
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