Nitric oxide regulation of asthmatic airway inflammation with segmental allergen challenge

1999 ◽  
Vol 27 ◽  
pp. S124
1999 ◽  
Vol 104 (6) ◽  
pp. 1174-1182 ◽  
Author(s):  
Mary Jane Thomassen ◽  
Baisakhi Raychaudhuri ◽  
Raed A. Dweik ◽  
Carol Farver ◽  
Lisa Buhrow ◽  
...  

Nitric Oxide ◽  
2005 ◽  
Vol 13 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Veit J. Erpenbeck ◽  
Rudolf A. Jörres ◽  
Marc Discher ◽  
Harald Krentel ◽  
Dimitrios Tsikas ◽  
...  

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.


Thorax ◽  
2015 ◽  
Vol 71 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Chris Carlsten ◽  
Anders Blomberg ◽  
Mandy Pui ◽  
Thomas Sandstrom ◽  
Sze Wing Wong ◽  
...  

RationaleTraffic-related air pollution has been shown to augment allergy and airway disease. However, the enhancement of allergenic effects by diesel exhaust in particular is unproven in vivo in the human lung, and underlying details of this apparent synergy are poorly understood.ObjectiveTo test the hypothesis that a 2 h inhalation of diesel exhaust augments lower airway inflammation and immune cell activation following segmental allergen challenge in atopic subjects.Methods18 blinded atopic volunteers were exposed to filtered air or 300 µg PM2.5/m3 of diesel exhaust in random fashion. 1 h post-exposure, diluent-controlled segmental allergen challenge was performed; 2 days later, samples from the challenged segments were obtained by bronchoscopic lavage. Samples were analysed for markers and modifiers of allergic inflammation (eosinophils, Th2 cytokines) and adaptive immune cell activation. Mixed effects models with ordinal contrasts compared effects of single and combined exposures on these end points.ResultsDiesel exhaust augmented the allergen-induced increase in airway eosinophils, interleukin 5 (IL-5) and eosinophil cationic protein (ECP) and the GSTT1 null genotype was significantly associated with the augmented IL-5 response. Diesel exhaust alone also augmented markers of non-allergic inflammation and monocyte chemotactic protein (MCP)-1 and suppressed activity of macrophages and myeloid dendritic cells.ConclusionInhalation of diesel exhaust at environmentally relevant concentrations augments allergen-induced allergic inflammation in the lower airways of atopic individuals and the GSTT1 genotype enhances this response. Allergic individuals are a susceptible population to the deleterious airway effects of diesel exhaust.Trial registration numberNCT01792232.


Radiology ◽  
2015 ◽  
Vol 274 (1) ◽  
pp. 267-275 ◽  
Author(s):  
Julius Renne ◽  
Jan Hinrichs ◽  
Christian Schönfeld ◽  
Marcel Gutberlet ◽  
Carla Winkler ◽  
...  

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