The monitoring of airway inflammation has assessed in bronchial asthma directly by sputum examination, and indirectly by measurements in peripheral blood. To investigate the diagnostic value of these two methods, we compared nitric oxide (NO) metabolites, eosinophils, and eosinophil cationic protein (ECP) in sputum and blood in patients with asthma and control subjects. Sputum and serum were obtained from fifteen patients with asthma, and then were examined before anti-asthma treatment, including steroid preparations. ECP was measured by fluoroimmunoassay. NO metabolites were assayed by using modified Griess reaction. Asthmatic patients, compared with control subjects, had significantly higher level of NO metabolites, higher proportion of eosinophils, and higher levels of ECP in sputum. Asthmatic patients, compared with control subjects, however, had significantly higher number of eosinophils, and were at higher levels of ECP in blood. FEV1, FEV1 /FVC was negatively correlated with sputum eosinophils. The area under receiver operating characteristic(ROC) curve showed that eosinophils in sputum are significantly accurate markers than NO metabolites in sputum and blood. These findings suggest that the proportion of eosinophils in sputum have more accurate diagnostic marker of asthmatic airway inflammation than NO metabolites in sputum in differentiating asthmatic patients from control subjects.
Adult ; Area Under Curve ; Asthma/*blood/*metabolism ; Blood Proteins/*metabolism ; Comparative Study ; Eosinophils/*metabolism ; Female ; Fluoroimmunoassay ; Human ; Inflammation ; Male ; Nitrates/metabolism ; Nitric Oxide/blood/*metabolism ; Nitrites/metabolism ; ROC Curve ; Ribonucleases/blood/*metabolism ; Sputum/*metabolism

OBJECTIVETo observe the effect of Pingchuan Mixture (PCM) on plasma eosinophil cation protein (ECP), interleukin-5 in bronchial alveolar lavage fluid (BALF) and inflammatory cell count in experimental guinea pigs with asthma.

METHODSThe eosinophil, neutrophil, lymphocyte count were conducted by conventional method, IL-5 was detected by ELISA and ECP determined by RIA.

RESULTSLevels of eosinophil, neutrophil, lymphocyte, ECP and IL-5 after treatment were significantly lower than those before treatment, the difference between groups treated respectively by PCM, aminophylline, dexamethasone and Dingchuan Zhike Tablet was insignificant.

CONCLUSIONPCM could treat asthma by reducing the inflammatory cell count, ECP and IL-5.

Animals ; Asthma ; chemically induced ; metabolism ; Blood Proteins ; metabolism ; Bronchoalveolar Lavage Fluid ; chemistry ; Drugs, Chinese Herbal ; pharmacology ; Eosinophil Granule Proteins ; Eosinophils ; metabolism ; Guinea Pigs ; Interleukin-5 ; metabolism ; Ovalbumin ; Ribonucleases ; metabolism

AIMTo evaluate the effect of interleukin-1 receptor antagonist(IL-1ra) on apoptosis and associated mechanism of eosinophil in guinea pig with asthma.

METHODSA model of guinea pig with asthma was established. After inhalation of different concentrations of IL-1ra, asthma was induced in the guinea pig for 8 days, the concentration of eosinophil cationic protein (ECP) in serum and bronchoalveolar lavage fluid (BALF), IL-5 in serum, the eosinophil counts and apoptosis were assayed by radioimmunology, enzyme-linked immunosorbent assay(ELISA), fluoromicroscope and light microscope.

RESULTSIL-1ra indirectly decreased the level of IL-5 in serum, improved the apoptosis of eosinophil(EOS) in lung, then decreased the level of ECP in serum and BALF.

CONCLUSIONInhalation of nebulized IL-1ra showed protective effect against asthma through change of the activity and infiltration of EOS in lung.

Animals ; Apoptosis ; Asthma ; blood ; chemically induced ; pathology ; Blood Proteins ; metabolism ; Bronchoalveolar Lavage Fluid ; chemistry ; Eosinophil Granule Proteins ; Eosinophils ; drug effects ; pathology ; Female ; Guinea Pigs ; Interleukin 1 Receptor Antagonist Protein ; Interleukin-5 ; blood ; Leukocyte Count ; Male ; Ovalbumin ; Random Allocation ; Receptors, Interleukin-1 ; antagonists & inhibitors ; Ribonucleases ; blood ; metabolism ; Sialoglycoproteins ; pharmacology

Eosinophil and mast cell infiltrations are consistent findings in nasal polyp tissue. Previous studies have shown that matrix metalloproteinases (MMPs) may be involved in eosinophil infiltration in airway mucosa of asthmatic patients, and that transforming growth factor-beta1 (TGF-beta1) induces extracellular matrix deposition in nasal polyp tissue. The aim of this study was to evaluate the role of MMPs and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in association with TGF-beta1, eosinophils and mast cell activation in nasal polyp tissue. Nasal polyp tissues from 20 patients who underwent polypectomies were collected and prepared into tissue homogenate. Eosinophil cationic protein (ECP) and tryptase levels were measured by CAP system (Pharmacia, Sweden). MMP-2, MMP-9, TIMP-1 and TGF-beta1 levels were measured by enzyme-liked immunosorbent assay. MMP-2 was the predominant form of MMPs, followed by MMP-9 and TIMP-1. There were significant correlations between ECP, and MMP-9, MMP-2, TGF-beta1 and tryptase, but not with TIMP-1. Significant correlations were noted between tryptase, and MMP-2, MMP-9, and TGF-beta1, but not with TIMP-1. Close correlations were noted between TGF-beta1, and MMP-9 and MMP-2, but not with TIMP-1. MMP-2, MMP-9, and TGF-beta1 may contribute to eosinophil and mast cell migrations into nasal polyp tissue.
Adult ; Asthma/complications ; Blood Proteins/analysis ; Chemotaxis, Leukocyte ; Eosinophilia/etiology ; Eosinophilia/metabolism* ; Eosinophilia/pathology ; Eosinophils/physiology ; Female ; Gelatinase A/analysis ; Gelatinase A/physiology* ; Gelatinase B/analysis ; Gelatinase B/physiology* ; Human ; Male ; Mast Cells/physiology ; Middle Aged ; Nasal Polyps/chemistry* ; Nasal Polyps/etiology ; Nasal Polyps/pathology ; Rhinitis/metabolism ; Rhinitis/pathology ; Ribonucleases* ; Serine Endopeptidases/analysis ; Tissue-Inhibitor of Metalloproteinase-1/analysis ; Tissue-Inhibitor of Metalloproteinase-1/physiology* ; Transforming Growth Factor beta/analysis ; Transforming Growth Factor beta/physiology*