Nitric oxide regulation of asthmatic airway inflammation with segmental allergen challenge☆,☆☆
Section snippets
Subjects
Six healthy control subjects and 8 patients with mild asthma were recruited for the study at the Cleveland Clinic (Table I).
Patient No. Age (y) Sex Baseline FEV1 (L) Baseline FEV1 (% predicted)13 A-PD20 by WLAC (PNU/mL) Maximum Ag by WLAC (PNU/mL) Fall in FEV1 at maximumAg (%) Ag for SAC SAC dose (PNU in 10 mL of NS) Asthmatic 1 29 F 2.89 88 1,000 1,000 –20 Grass 100 2 44 F 2.58 98 2,455 3,162 –21 Grass 300 3 40 F 3.05 100 232 316 –28 Grass 30 4 38 F 2.74 97 250 316 –25 Grass 100 5 31 F 3.37 96 1,441 3,162 –40 Grass
Inflammatory cells
At baseline the BALs from the healthy control subjects and the asthmatic patients were not different in total cell recovery, viability, or cellular differential (Table II). The allergen-challenged segment from the asthmatic group had a significant increase in the percent of eosinophils at 48 hours (P = .02, t test) and a corresponding decrease in the percent of macrophages. However, the absolute number of macrophages was slightly increased (Table II). Fig 1 shows the increase in eosinophils
DISCUSSION
The relationship between NO and asthma has not been conclusively defined. Airway NO levels in asthmatic patients are heterogeneous, with some patients in the same range as healthy control subjects. Whether this variation in airway NO levels corresponds to disease activity is not known. All the patients in the current study had mild asthma. Allergen-induced late asthmatic reactions have been associated with increased exhaled NO.20 Glucocorticoids decrease exhaled NO.5 Beneficial effects of
Acknowledgements
We thank Rita Piccin for recruiting and patient scheduling, Daniel Laskowski for assistance with airway NO measurements, Marusia Oleksiuk for allergen preparation, and Marc Lewis and Suzy Comhair for performing the urea assays.
References (28)
- et al.
Differential regulation of human blood monocyte and alveolar macrophage inflammatory cytokine production by nitric oxide
Ann Allergy Asthma Immunol
(1999) - et al.
Standardization of bronchial inhalation challenge procedures
J Allergy Clin Immunol
(1975) - et al.
Role of bronchoscopy in asthma research
Clin Chest Med
(1999) - et al.
Randomised double-blind placebo-controlled study of the effect of inhibition of nitric oxide synthesis in bradykinin-induced asthma
Lancet
(1996) Exhaled nitric oxide as a marker in asthma
Eur Respir J
(1998)- et al.
Nitric oxide and inflammation: the answer is blowing in the wind
Nat Med
(1997) - et al.
Changes in the dose of inhaled steroid affect exhaled nitric oxide levels in asthmatic patients
Eur Respir J
(1996) - et al.
Expired nitric oxide levels during treatment of acute asthma
Am J Respir Crit Care Med
(1995) - et al.
Inhaled glucocorticoids decrease nitric oxide in exhaled air of asthmatic patients
Am J Respir Crit Care Med
(1996) - et al.
Inhalation of nitric oxide modulates adult human bronchial tone
Am Rev Respir Dis
(1993)
Inhaled nitric oxide: a bronchodilator in mild asthmatics with methacholine-induced bronchospasm
Am J Respir Crit Care Med
Nitric oxide inhibits inflammatory cytokine production by human alveolar macrophages
Am J Respir Cell Mol Biol
The role of MIP-1a inflammation and hematopoiesis
J Leukoc Biol
Regulation of human eosinophil viability, density and function by granulocyte-macrophage colony-stimulating factor in the presence of 3T3 fibroblasts
J Exp Med
Cited by (49)
Bu-Shen-Yi-Qi formula ameliorates airway remodeling in murine chronic asthma by modulating airway inflammation and oxidative stress in the lung
2019, Biomedicine and PharmacotherapyCitation Excerpt :In addition, SOD activity did not increase as expected with BSYQF treatment that suggested that recovery of GSH may be a dominant effect by BSYQF treatment. Overproduction of NO can amplify and persist the Th2-mediated inflammatory response in asthma [51]. In human study, NO measurements were positively correlated with severity of airway remodeling in patients with refractory asthma [52].
Mitochondrial reactive oxygen species regulate fungal protease-induced inflammatory responses
2017, ToxicologyCitation Excerpt :In contrast, disproportionate formation of ROS causes tissue damage (Bhattacharyya et al., 2014). The role of multiple source-derived ROS, such as NADPH oxidase-derived ROS (Kim et al., 2012), XO generating ROS (Heunks et al., 1999; Ward, 2010) and NO generating ROS (Dotsch et al., 1996; Thomassen et al., 1999) in airway inflammation, have been massively studied. Although mitochondria are known to be one of major sources of intracellular ROS (Dikalov, 2011), functional significance of mitochondrial ROS has not been fully examined due to the lack of information for regulation of mitochondria ROS comparing to other ROS.
An inverse relationship between peroxisome proliferator-activated receptor γ and allergic airway inflammation in an allergen challenge model
2005, Annals of Allergy, Asthma and ImmunologyLocal nitric oxide levels reflect the degree of allergic airway inflammation after segmental allergen challenge in asthmatics
2005, Nitric Oxide - Biology and Chemistry
- ☆
Reprint requests: Mary Jane Thomassen, PhD, Department of Pulmonary and Critical Care Medicine, Cleveland Clinic Foundation, Desk A90, 9500 Euclid Ave, Cleveland, OH 44195-5038.
- ☆☆
0091-6749/99 $8.00 + 0 1/1/102215