Lower Airway Inflammation in Eosinophilic Chronic Rhinosinusitis as Determined by Exhaled Nitric Oxide

2017 ◽  
Vol 173 (4) ◽  
pp. 225-232 ◽  
Author(s):  
Rumi Kambara ◽  
Takafumi Minami ◽  
Hitoshi Akazawa ◽  
Fumio Tsuji ◽  
Takanobu Sasaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Airway Inflammation ◽  
Chronic Rhinosinusitis ◽  
Exhaled Nitric Oxide ◽  
Lower Airway ◽  
Eosinophilic Chronic Rhinosinusitis

scholarly journals Reduced Local Response to Corticosteroids in Eosinophilic Chronic Rhinosinusitis with Asthma

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 326 ◽  
Author(s):  
Yoshiki Kobayashi ◽  
Akira Kanda ◽  
Yasutaka Yun ◽  
Dan Van Bui ◽  
Kensuke Suzuki ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Nuclear Translocation ◽  
Uncinate Process ◽  
Lower Airway ◽  
Mrna Levels ◽  
Eosinophilic Chronic Rhinosinusitis ◽  
Key Factor

Eosinophilic chronic rhinosinusitis (ECRS), a subgroup of chronic rhinosinusitis with nasal polyps, is recognized as a refractory eosinophilic disorder characterized by both upper and lower airway inflammation. In some severe cases, disease control is poor, likely due to local steroid insensitivity. In this study, we focused on protein phosphatase 2A (PP2A), a key factor regulating glucocorticoid receptor (GR) nuclear translocation, and examined its association with local responses to corticosteroids in eosinophilic airway inflammation. Our results indicated reduced responses to corticosteroids in nasal epithelial cells from ECRS patients with asthma, which were also associated with decreased PP2A mRNA expression. Eosinophil peroxidase stimulates elevated PP2A phosphorylation levels, reducing PP2A protein expression and activity. In addition, mRNA levels of inflammatory mediators (TSLP, IL-25, IL-33, CCL4, CCL5, CCL11, and CCL26) associated with eosinophilic airway inflammation in epithelial cells were increased in nasal polyps (eosinophil-rich areas) compared with those in uncinate process tissues (eosinophil-poor areas) from the same patients. PP2A reduction by siRNA reduced GR nuclear translocation, whereas PP2A overexpression by plasmid transfection, or PP2A activation by formoterol, enhanced GR nuclear translocation. Collectively, our findings indicate that PP2A may represent a promising therapeutic target in refractory eosinophilic airway inflammation characterized by local steroid insensitivity.

scholarly journals Residual exhaled nitric oxide elevation in asthmatics is associated with eosinophilic chronic rhinosinusitis

2015 ◽  
Vol 52 (10) ◽  
pp. 1060-1064 ◽  
Author(s):  
Yoshiki Kobayashi ◽  
Mikiya Asako ◽  
Hisashi Ooka ◽  
Akira Kanda ◽  
Koichi Tomoda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chronic Rhinosinusitis ◽  
Exhaled Nitric Oxide ◽  
Eosinophilic Chronic Rhinosinusitis

Increased exhaled nitric oxide and its oxidation metabolism in eosinophilic chronic rhinosinusitis

2013 ◽  
Vol 40 (5) ◽  
pp. 458-464 ◽  
Author(s):  
Sachio Takeno ◽  
Takayuki Taruya ◽  
Tsutomu Ueda ◽  
Noriaki Noda ◽  
Katsuhiro Hirakawa
Keyword(s):  
Nitric Oxide ◽  
Chronic Rhinosinusitis ◽  
Exhaled Nitric Oxide ◽  
Eosinophilic Chronic Rhinosinusitis

Exhaled Nitric Oxide Predicts Eosinophilic Airway Inflammation in COPD

Lung ◽  
2014 ◽  
Vol 192 (4) ◽  
pp. 499-504 ◽  
Author(s):  
Kun-Ta Chou ◽  
Kang-Cheng Su ◽  
Shiang-Fen Huang ◽  
Yi-Han Hsiao ◽  
Ching-Min Tseng ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Airway Inflammation ◽  
Exhaled Nitric Oxide

Exhaled nitric oxide estimation by a simple and efficient noninvasive technique and its utility as a marker of airway inflammation in mice

2009 ◽  
Vol 107 (1) ◽  
pp. 295-301 ◽  
Author(s):  
Tanveer Ahmad ◽  
Ulaganathan Mabalirajan ◽  
Duraisamy Arul Joseph ◽  
Lokesh Makhija ◽  
Vijay Pal Singh ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Airway Inflammation ◽  
Airway Remodeling ◽  
Allergen Challenge ◽  
Allergic Airway Inflammation ◽  
Ambient Air ◽  
Exhaled Nitric Oxide ◽  
Noninvasive Technique ◽  
Modified Method ◽  
Chronic Models

Allergic airway inflammation (AI) is commonly associated with enhanced exhaled nitric oxide (ENO) in both humans and mice. Since mouse models are being used to understand various mechanisms of asthma, a noninvasive, simple, and reproducible method to determine ENO in mice is required for serial nonterminal assessment that can be used independent of environmental situations in which the ambient air contains substantial amounts of NO as a contaminant. The aim of this study was to noninvasively measure ENO in individual mice and to test its utility as a marker of AI in different models of allergic AI. We modified the existing ENO measuring methods by incorporating flushing and washout steps that allowed simple but reliable measurements under highly variable ambient NO conditions (1–100 ppb). This method was used to serially follow ENO in acute and chronic models of allergic AI in mice. ENO was reproducibly measured by this modified method and was positively correlated to AI in both acute and chronic models of asthma but was not independently related to airway remodeling. Resolution of AI and other related parameters in dexamethasone-treated mice resulted in reduction of ENO, further confirming this association. Restriction of allergen challenge to pulmonary but not nasal airways was associated with a smaller increase in ENO compared with allergen challenge to both. Hence, ENO can now be reliably measured in mice independent of ambient NO levels and is a valid biomarker for AI. However, nasal and pulmonary airways are likely to be independent sources of ENO, and any results must be interpreted as such.

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