Useful exhaled nitric oxide measures to evaluate the deleterious effect of home environment on airway inflammation in an asthmatic child

Author(s):  
Mitsuhiro Nishida ◽  
Shigemi Yoshihara
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 ◽  
...  

2009 ◽  
Vol 107 (1) ◽  
pp. 295-301 ◽  
Author(s):  
Tanveer Ahmad ◽  
Ulaganathan Mabalirajan ◽  
Duraisamy Arul Joseph ◽  
Lokesh Makhija ◽  
Vijay Pal Singh ◽  
...  

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.


2014 ◽  
Vol 35 (3) ◽  
pp. 241-249 ◽  
Author(s):  
M. Asghar Pasha ◽  
David Jourd'heuil ◽  
Francis Jourd'heuil ◽  
Lori Mahon ◽  
Francisco Romero ◽  
...  

Author(s):  
Rebekka F Thudium ◽  
Nicolai L P Hughes ◽  
Shoaib Afzal ◽  
Yunus Çolak ◽  
Marco Gelpi ◽  
...  

Abstract Background Increased risk of asthma and chronic obstructive pulmonary disease has been reported in people living with human immunodeficiency virus (PLWH). Fraction of exhaled nitric oxide (FeNO) is a marker of eosinophilic airway inflammation. We assessed FeNO levels in PLWH and matched uninfected controls and investigated whether human immunodeficiency virus (HIV) status is independently associated with elevated FeNO. Methods FeNO was quantified by NIOX Vero and pulmonary function was assessed by spirometry in 432 PLWH from the Copenhagen Comorbidity in HIV Infection Study and in 1618 age- and sex-matched uninfected controls from the Copenhagen General Population Study. Elevated FeNO was defined as ≥25 parts per billion. Associations between FeNO and HIV status were adjusted for known potential confounders. Results Mean age of PLWH was 50.7 (standard deviation [SD], 11.1) years and 97.4% received combination antiretroviral therapy. PLWH had higher FeNO than uninfected controls (median, 17.0 [interquartile range {IQR}, 11.0–26.0] vs 13.0 [IQR, 9.0–19.0]; P < .001). Also, PLWH had a higher prevalence of elevated FeNO than uninfected controls (27.5% vs 12.3%; P < .001). This association remained after adjusting for age, sex, height, smoking status, use of airway medication, blood eosinophils, and immunoglobulin E (adjusted OR [aOR], 3.56 [95% CI, 2.51–5.04]; P < .001). Elevated FeNO was associated with self-reported asthma (aOR, 2.65 [95% CI, 1.66–4.24]; P < .001) but not with airflow limitation (aOR, 1.07 [95% CI, .71–1.62]; P = .745). Conclusions HIV status was independently associated with elevated FeNO, suggesting increased eosinophilic airway inflammation. The potential impact on chronic lung disease pathogenesis needs further investigation.


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