MUCUS SECRETION AND ITS ROLE IN DEFENCE REFLEXES

Respiration ◽  
1981 ◽  
pp. 519-528
Author(s):  
A.C. Peatfield
Keyword(s):  
2001 ◽  
Vol 120 (5) ◽  
pp. A675-A675
Author(s):  
F TOUMI ◽  
J CLAUSTRE ◽  
A TROMPETTE ◽  
G JOURDAN ◽  
H GUIGNARD ◽  
...  
Keyword(s):  

2006 ◽  
Vol 101 (2) ◽  
pp. 486-491 ◽  
Author(s):  
Jung-Soo Kim ◽  
Kosuke Okamoto ◽  
Shinobu Arima ◽  
Bruce K. Rubin

Vasoactive intestinal peptide (VIP) and nitric oxide (NO) are neurotransmitters involved in the regulation of bronchial and pulmonary vascular tone. Published studies of the effects of VIP on airway mucus secretion have yielded conflicting results. The purpose of this study was to determine the effect of VIP on mucus secretion in the ferret trachea and if this effect was influenced by NO. We used a sandwich enzyme-linked lectin assay to measure mucin secretion and a turbidimetric assay to measure lysozyme (serous cell) secretion from ferret tracheal segments. VIP (10−7 M) increased mucin secretion over 2 h. VIP (10−9 to 10−5 M) stimulated mucin secretion in a dose-dependent fashion. VIP-induced mucin secretion was partially blocked by a VIP receptor antagonist (a chimeric VIP-pituitary adenylate cyclase-activating peptide analog, VIP receptor antagonist) at a 10-fold excess concentration. At all concentrations tested, neither NG-nitro-l-arginine methyl ester, an inhibitor of NO synthase, nor S-nitroso- N-acetyl-penicillamine, an NO donor, had any significant effect on constitutive or VIP-induced mucus secretion. We conclude that VIP-stimulated mucin and lysozyme secretion was both time dependent and dose dependent and that NO neither stimulates nor inhibits mucus secretion in the ferret trachea.


2010 ◽  
Vol 9 ◽  
pp. S18
Author(s):  
H.-J. Lee ◽  
H.-J. Cho ◽  
D.-M. Shin ◽  
N.-S. Joo ◽  
J.-Y. Choi

2021 ◽  
Author(s):  
Varsha Singh ◽  
Kelli Johnson ◽  
Jianyi Yin ◽  
Sunny Lee ◽  
Ruxian Lin ◽  
...  

ABSTRACTObjectiveOne of the features of ulcerative colitis (UC) is a defect in the protective mucus layer. This has been attributed to a reduced number of goblet cells (GC). However, it is not known whether abnormal GC mucus secretion also contributes to the reduced mucus layer. Our aims were to test the hypothesis that GC secretion was abnormal in UC with the changes persistent in colonoids even in the absence of immune cells.DesignColonoids were established from intestinal stem cells of healthy subjects (HS) and from patients with UC (inactive and active sites). Colonoids were maintained as undifferentiated (UD) or induced to differentiate (DF) and studied as 3D or monolayers on Transwell filters. Total RNA was extracted for quantitative real-time PCR analysis. Carbachol and PGE2 mediated stimulation followed by examination of mucus layer by MUC2 IF/confocal microscopy and TEM were performed.ResultsColonoids derived from patients with UC can be propagated over many passages; however, they exhibit a reduced rate of growth and TEER compared with colonoids from HS. Differentiated UC colonoid monolayers form a thin and non-continuous mucus layer. UC colonoids have increased expression of secretory lineage markers: ATOH1 and SPDEF, including MUC2 positive GCs and ChgA positive enteroendocrine cells but failed to secrete mucin when exposed to the cholinergic agonist carbachol and PGE2, which caused increased secretion in HS. Exposure to TNF-α (5days), reduced the number of GC with a greater percentage decrease in UC colonoids compared to HS.ConclusionsAbnormal mucus layer in UC is due to long term changes in epithelial cells that lead to abnormal mucus secretion as well as effects of the inflammatory environment to reduce the number of GC. This continued defect in GC mucus secretion may be involved in UC recurrence.


2018 ◽  
Vol 36 (5) ◽  
pp. 319-326 ◽  
Author(s):  
Ming Dong ◽  
Cheng Ma ◽  
Wen-Qian Wang ◽  
Juan Chen ◽  
Ying Wei

Background Bronchial asthma is a chronic airway inflammatory disease which has three main pathological features: airway hyperresponsiveness (AHR), airway remodelling, and chronic inflammation. Acupuncture is known to be an effective integrative medical therapy that has been used in the treatment of several chronic diseases, including bronchial asthma. The aim of the current study was to evaluate the effects of acupuncture on inflammation and regulation of the IL-33/ST2 pathway in a mouse model of asthma. Methods The murine asthma model was established by both injection and inhalation of ovalbumin (OVA). Within 24 hours of the last OVA challenge, lung function was assessed by measurement of the airway resistance (RL) and lung dynamic compliance (Cdyn). Pulmonary tissues were collected for the detection of pathological changes and mucus secretion. Serum levels of tumour necrosis factor α (TNF-α), interleukin (IL)-1β, IL-33 and sST2 (secreted ST2) were detected by ELISA. Th17 cell proportions and counts in bronchoalveolar lavage fluid (BALF) were analysed by flow cytometry. Results The results showed that AHR, chronic inflammation and mucus secretion were significantly suppressed by acupuncture treatment. RL decreased while Cdyn increased after acupuncture treatment. There was an apparent decrease in the serum concentrations of certain pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-33, and an increase in sST2 level compared with untreated asthmatic mice. Acupuncture also reduced the CD4 +IL-17A+ cell proportion and counts in BALF. Conclusion Acupuncture effectively protects lung function and attenuates airway inflammation in the OVA-induced mouse model of asthma, which supports the role of acupuncture as a potential therapy in asthma treatment.


1992 ◽  
Vol 58 ◽  
pp. 236
Author(s):  
Hirofumi Kai ◽  
Kazuhisa Yoshitake ◽  
Ichiro Hamamura ◽  
Yoichiro Isohama ◽  
Kazuo Takahama ◽  
...  
Keyword(s):  

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