scholarly journals Photoacoustic technique: a new method for measuring the rheologic properties of human bronchial mucus

2019 ◽  
Vol 6 ◽  
Author(s):  
Luis V.F. De Oliveira ◽  
Newton S. De Faria Jr. ◽  
Fernanda M. Garcia Gonzaga Napoleone ◽  
Marcelo A. Ingraci Barboza ◽  
Fernando S. Studart Leitão Filho ◽  
...  

Patients affected by obstructive pulmonary diseases exhibit typical characteristics of airway mucus hypersecretion, including sputum production, in- creased luminal mucus, goblet cell hyperplasia and submucosal gland hypertrophy. The mucociliary system is a sophisticated defense mechanism to maintain the homeostasis of the respiratory tract by means of the bronchial mucus transport, the process in which airway mucus together with substances trapped within are moved out of the lungs. In the end, the mucus together with the substances trapped within are swallowed or coughed up. It is an impor- tant defense mechanism of the human body. [...]


2020 ◽  
Author(s):  
Feng Feng ◽  
Changle Zhu ◽  
Yufeng Meng ◽  
Fang Guo ◽  
Cuiling Feng

Abstract Background Exposure to fine particulate matter (PM2.5) severely impairs public health. The mechanism of PM2.5-induced lung injury is complex and diverse. Modified Guo-Min Decoction (MGMD) and Yu-Ping-Feng Powder (YPFP) have been found to improve clinical symptoms in respiratory patients during smog weather, but the mechanism remains unclear. This study aimed to investigate the effect and mechanism of YPFP and MGMD against PM2.5-induced lung injury. Methods We established the PM2.5 animal model by intratracheal instilling of PM2.5 suspensions. Rats were administrated MGMD/YPFP/distilled water via gavage every day, and all rats were sacrificed after 28 days. At the end of experiment, BALF and lung tissues were collected. Condition of lung injury, inflammatory cells infiltration, inflammatory cytokines, MUC5AC synthesis and release, and phosphorylation of TLR2-MyD88-NFκB and EGFR-PI3K-AKT signalling pathway were evaluated. Results The results demonstrated that both MGMD and YPFP protected rats from PM2.5-induced damaged structure of lung tissues. The infiltration of neutrophil, monocyte, lymphocyte, and eosinophil was reduced after the treatment of two therapies. The production of pro-inflammatory mediators, MCP-1 and NE, as well as the type2 inflammation-related cytokines, IgE and IL-4, were decreased by MGMD and YPFP. However, the MGMD showed more potent effect on inhibiting IL-4, while YPFP benefited in preventing ICMA-1, IL-1β, and IL-17A. Rare significance was detected in the TLR2-MyD88-NFκB of each group. Treatment with MGMD and YPFP decreased goblet cell hyperplasia and the expressions of MUC5AC. The further investigation demonstrated that YPFP had the effect of simultaneously inhibiting the phosphorylation of PI3K and AKT, whereas MGMD only showed a significant difference in AKT. Conclusions Therefore, both MGMD and YPFP could significantly attenuate PM2.5-induced inflammation of lung and airway mucus hypersecretion. Nevertheless, YPFP had more advantage in preventing type1 inflammation and mucus hypersecretion, while MGMD was more beneficial in reducing type2 inflammation.





2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Huanhuan Zhang ◽  
Wenying Yu ◽  
Liting Ji ◽  
Yusen Zhong ◽  
Yiyou Lin ◽  
...  

Mucus hypersecretion is a hallmark of chronic obstructive pulmonary disease (COPD) and is associated with increasing sputum production and declining pulmonary function. Therefore, reducing mucus secretion can be a new therapeutic opportunity for preventing COPD. The Guifu Dihuang pill (GFDHP) is a classical Chinese medicine and has been used as an immunoregulator for treatment of kidney yang deficiency syndrome, including hypothyroidism, adrenocortical hypofunction, chronic bronchitis, and COPD, for more than 2000 years. However, the protective effects and mechanisms of GFDHP against mucus hypersecretion in COPD remain obscure. The aim of the present study was to explore the inhibitory effects of GFDHP on lipopolysaccharide/cigarette smoke- (LPS/CS-) induced Mucin5ac (Muc5ac) overproduction and airway goblet cell hyperplasia in mice. The mice were randomly assigned into 6 groups: control, model, GFDHP-L, GFDHP-M, GFDHP-H, and dexamethasone. The mice were given LPS twice through intranasal inhalation and then exposed to CS daily for 6 weeks. Three doses of GFDHP were orally administered daily during the last 3 weeks of the experiment. Pulmonary function was examined with an EMKA pulmonary system, and pulmonary hyperpermeability and lung damage were evaluated with an in vivo imaging system. Inflammatory cells and cytokines in bronchoalveolar lavage fluid (BALF) were detected with a cell count analyzer and though ELISA analysis, respectively. Lung pathological changes and airway goblet cell hyperplasia were analyzed with hematoxylin and eosin and Alcian blue periodic acid Schiff staining. The protein expression levels of Muc5ac and extracellular signal-regulated kinase (ERK)-specificity protein1 (SP1) signaling pathway were measured with Western blot and immunohistochemistry. The results demonstrated that GFDHP improved pulmonary function and suppressed mouse pulmonary hyperpermeability and edema. GFDHP suppressed inflammatory cell infiltration and cytokine release in BALF, thereby elevating pulmonary function. It ameliorated lung pathological changes and airway goblet cell hyperplasia, and suppressed expression levels of Muc5ac mRNA and protein and phospho-ERK and SP1 levels in the lung tissues of the COPD mice. In conclusion, GFDHP inhibited mucus hypersecretion induced by LPS/CS by suppressing the activation of the ERK-SP1 pathway.



2012 ◽  
Vol 101 (12) ◽  
pp. 3525-3532 ◽  
Author(s):  
Mitsuko Kondo ◽  
Jun Tamaoki


Author(s):  
Paula J. Busse ◽  
John V. Fahy


2014 ◽  
pp. 739-753
Author(s):  
Duncan F. Rogers


2019 ◽  
Vol 116 (51) ◽  
pp. 25697-25706 ◽  
Author(s):  
Hyun-Taek Kim ◽  
Wenguang Yin ◽  
Yuko Nakamichi ◽  
Paolo Panza ◽  
Beate Grohmann ◽  
...  

Goblet cell metaplasia and mucus hypersecretion are observed in many pulmonary diseases, including asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis. However, the regulation of goblet cell differentiation remains unclear. Here, we identify a regulator of this process in anN-ethyl-N-nitrosourea (ENU) screen for modulators of postnatal lung development;Rykmutant mice exhibit lung inflammation, goblet cell hyperplasia, and mucus hypersecretion. RYK functions as a WNT coreceptor, and, in the developing lung, we observed high RYK expression in airway epithelial cells and moderate expression in mesenchymal cells as well as in alveolar epithelial cells. From transcriptomic analyses and follow-up studies, we found decreased WNT/β-catenin signaling activity in the mutant lung epithelium. Epithelial-specificRykdeletion causes goblet cell hyperplasia and mucus hypersecretion but not inflammation, while club cell-specificRykdeletion in adult stages leads to goblet cell hyperplasia and mucus hypersecretion during regeneration. We also found that the airway epithelium of COPD patients often displays goblet cell metaplastic foci, as well as reduced RYK expression. Altogether, our findings reveal that RYK plays important roles in maintaining the balance between airway epithelial cell populations during development and repair, and that defects in RYK expression or function may contribute to the pathogenesis of human lung diseases.



1996 ◽  
Vol 71 ◽  
pp. 28
Author(s):  
Yoshiaki Inayama ◽  
Satoshi Asano ◽  
Masayoshi Kanisawa


Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2869 ◽  
Author(s):  
Kalahe Hewage Iresha Nadeeka Madushani Herath ◽  
Hyo Jin Kim ◽  
Areum Kim ◽  
Chung Eui Sook ◽  
Boo-Yong Lee ◽  
...  

Ambient particulate matter (PM) is a critical environment pollutant that promotes the onset and aggravation of respiratory diseases such as asthma through airway inflammation and hypersecretion of mucus. In this study, we aimed to identify the effects of fucoidans isolated from sporophylls of Undaria pinnatifida on asthma symptoms such as the inflammatory response and mucus secretion using a mouse model. Balb/c mice, intraperitoneally sensitized with ovalbumin (OVA, 10 μg) dissolved in 200 µL saline and 2 mg Al(OH)3, were exposed to PM (5 mg/m3) for 7 consecutive days. In parallel, along with PM exposure, we orally administrated fucoidans (100, 400 mg/Kg) or prednisone (5 mg/Kg), an anti-inflammatory drug. We found that oral administration of fucoidans significantly attenuated PM-induced lipid peroxidation and infiltration of inflammatory cells like F4/80+ macrophages, Gr-1+ granulocytes, and CD4+ T lymphocytes. Fucoidans also attenuated the level of PM-exacerbated IL-4, a primitive cytokine released in Th2 mediated eosinophilic asthma. This further suppressed mast cell activation, degranulation and IgE synthesis of PM exposed mice. Interestingly, fucoidans attenuated PM-exacerbated mucus hypersecretion and goblet cell hyperplasia. Therefore, our results suggest that fucoidans are effective at alleviating PM-exacerbated allergic asthma symptoms by attenuating the airway inflammatory response and mucus hypersecretion.



PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Yongchun Shen ◽  
Lei Chen ◽  
Tao Wang ◽  
Fuqiang Wen

Airway mucus hypersecretion (AMH) is a key pathophysiological feature of chronic airway inflammatory diseases such as bronchial asthma, cystic fibrosis, and chronic obstructive pulmonary disease. AMH contributes to the pathogenesis of chronic airway inflammatory diseases, and it is associated with reduced lung function and high rates of hospitalization and mortality. It has been suggested that AMH should be a target in the treatment of chronic airway inflammatory diseases. Recent evidence suggests that a key regulator of airway inflammation, hyperresponsiveness, and remodeling is peroxisome proliferator-activated receptor gamma (PPARγ), a ligand-activated transcription factor that regulates adipocyte differentiation and lipid metabolism. PPARγis expressed in structural, immune, and inflammatory cells in the lung. PPARγis involved in mucin production, and PPARγagonists can inhibit mucin synthesis bothin vitroandin vivo. These findings suggest that PPARγis a novel target in the treatment of AMH and that further work on this transcription factor may lead to new therapies for chronic airway inflammatory diseases.



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