Pared to the other two groups. As we expected, the Calv levels in the EP group (14.4 ?2.0 ppb) were markedly higher than in the healthy subject (5.1 ?0.6 ppb, p < 0.01) and the IPF groups (6.3 ?0.6 ppb, p < 0.01, Figure 1B). JawNO was also calculated with a two compartment model. There was no significant difference among the three groups (Figure 1C). To avoid the influence of contamination from NO produced in the airways to Calv, we also calculated the corrected Calv. The corrected Calv levels in the EP group (13.3 ?2.0 ppb) were significantly higher than those in both the healthy subjects (4.5 ?0.6 ppb, p < 0.01) and the IPF groups (5.3 ?0.6 ppb, p < 0.01, Figure 1D).iNOS expression and nitrosative stress in EPEBCs were obtained from nine healthy subjects, eleven IPF patients and nine EP patients. We examined the expression of 42 different cytokines in EBC using a cytokine assay method. The cytokine and chemokine profiling are summarized in Additional file 4, Table S3. There was no significant difference in their expression among the 3 groups.The effects of corticosteroid treatment on nitrosative stress in the patients with EPCell differential counts in the BALf of the study subjects are listed in Additional file 2, Table S1. To investigate the source of increased NO production in the exhaled air from the patients with EP, we performed immunostaining for iNOS in the BALf cells. More iNOS positive cells were observed in the patients with EP than in the healthy subject and IPF patient (Figure 2A-C, Additional file 3, Table S2). There were significant positive correlations between the proportion of iNOS positive cells and the FENO levels (r = 0.913, p < 0.01, Figure 2D), JawNO levels (r = 0.869, p < 0.05), or the Calv levels (r = 0.858, p < 0.05, Figure 2E). More 3-NT positive cells were alsoTo elucidate whether the exhaled NO levels in EP changes during systemic corticosteroid treatment, we measured the exhaled NO levels as well as lung function and systemic inflammatory markers before/after treatment with systemic corticosteroid. All patients' symptoms and chest radiographic findings were completely improved by corticosteroid treatment for 4 weeks. After corticosteroid treatment, the FE NO (44.1 ?4.7 ppb vs 27.3 ?2.1 ppb, p < 0.05) and the Calv levels (15.1 ?2.4 ppb vs 6.90 ?0.87 ppb, p < 0.01) were significantly reduced (Table 3). As expected, among the lung function tests, the VC (2.46 ?0.38 L vs 2.96 ?0.34 L, p < 0.01) and VC (83.6 ?11 vs 100 ?11 , p < 0.01) values were significantly restored (Table 3). Peripheral blood eosinophil counts (584 ?210/l vs 45.4 ?13/l, p < 0.01) and CRP levels (1.91 ?1.0 mg/dl vs 0.348 ?0.29 mg/dl, p < 0.05) were also significantly reduced (Table 3). To determine whether the exhaled NO reflects the lung inflammation in EP, we investigated the correlation between the degree of reduction in the exhaled NO levels and those in the values of PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26577270 lung function Trichostatin A site andFurukawa et al. Respiratory Research 2011, 12:81 http://respiratory-research.com/content/12/1/Page 5 of(A)80 60 40 20p<0.01 p<0.01 N.S.(B)p<0.01 p<0.01 N.S.FENO (ppb)Calv (ppb)HSIPFEPHSIPFEP(C)2.5 JawNO (nl/s) 2.0 1.5 1.0 0.5 0 HSN.S.N.S. N.S.(D)30 Corrected Calv (ppb)p<0.01 p<0.01 N.S.0 IPF EPHSIPFEPFigure 1 Exhaled nitric oxide (NO) levels in the study subjects. Panels show the fractional exhaled NO (FENO) levels (A), the alveolar NO (Calv) levels (B), airway wall NO (JawNO) (C), and corrected Calv (D). Horizontal lines represent the mean value of the.
