The nose is an attractive source of airway epithelial cells, particularly in populations in which bronchoscopy may not be possible. However, substituting nasal cells for bronchial epithelial cells in the study of airway inflammation depends upon comparability of responses, and evidence for this is lacking. Our objective was to determine whether nasal epithelial cell inflammatory mediator release and receptor expression reflect those of bronchial epithelial cells. Paired cultures of undifferentiated nasal and bronchial epithelial cells were obtained from brushings from 35 subjects, including 5 children. Cells were subject to morphologic and immunocytochemical assessment. Mediator release from resting and cytokine-stimulated cell monolayers was determined, as was cell surface receptor expression. Nasal and bronchial cells had identical epithelial morphology and uniform expression of cytokeratin 19. There were no differences in constitutive expression of CD44, intercellular adhesion molecule-1, alphavbeta3, and alphavbeta5. Despite significantly higher constitutive release of IL-8, IL-6, RANTES (regulated on activation, normal T cell expressed and secreted), and matrix metalloproteinase (MMP)-9 from nasal compared with bronchial cells, the increments in release of all studied mediators in response to stimulation with IL-1beta and TNF-alpha were similar, and there were significant positive correlations between nasal and bronchial cell secretion of IL-6, RANTES, vascular endothelial growth factor, monocyte chemoattractant protein-1, MMP-9, and tissue inhibitor of metalloproteinase-1. Despite differences in absolute mediator levels, the responses of nasal and bronchial epithelial cells to cytokine stimulation were similar, expression of relevant surface receptors was comparable, and there were significant correlations between nasal and bronchial cell mediator release. Therefore, nasal epithelial cultures constitute an accessible surrogate for studying lower airway inflammation.
Abstractnot differ from men in Symptom scores on the SGRQ but differed markedly on the Background -There is some evidence that Activity and Impact scales. quality of life (QOL) in patients withConclusions -It is concluded that poor chronic obstructive pulmonary disease scores on the SGRQ, a QOL scale which (COPD) may predict clinical outcomes measures patient distress and coping, are and use of resources. This study examined associated with re-admission for COPD whether QOL scores could prospectively and use of resources such as nebulisers, predict re-admission for COPD or death independent of physiological measures of within 12 months of an original admission, disease severity. and whether QOL scores predicted home (Thorax 1997;52:67-71) nebuliser provision. Methods -The study was carried out in all acute medical wards of Aberdeen Royal Keywords: chronic obstructive pulmonary disease, hospital admission, quality of life.Infirmary, Woodend and City Hospitals, Aberdeen over 12 months. A total of 377 patients admitted with an exacerbation of COPD were identified in this time, 111 Quality of life (QOL) scales assess the impact of whom were not included in the study of illness and experience of health among inbecause they refused the interview or died dividuals. These scales include general "well before discharge. The remaining 266 being" measures such as the Sickness Impact patients completed the St George's Res-Profile (SIP) 1 and the General Health Survey piratory Questionnaire (SGRQ). In-(SF-36) 2 and measures especially designed for formation on spirometric parameters, respiratory disease such as the Chronic Resnebuliser provision at discharge, provision piratory Questionnaire (CRQ) 3 and the St of domiciliary oxygen, and re-admission George's Respiratory Questionnaire (SGRQ). patient's experience of symptoms, how far Results -The mean age of the patients was symptoms such as breathlessness limit daily life 68 years and 53% were men. The mean activity, and how much distress the disease (SD) forced expiratory volume in one sec-causes the patient.5 6 Jones et al 7 argue that ond (FEV 1 ) was 38.8 (18.0)% predicted and QOL measures are particularly relevant to the forced vital capacity (FVC) was 58.9 management of patients with chronic ob-(23.8)% predicted. Higher (worse) scores structive pulmonary disease (COPD) because on the SGRQ were significantly related to much of this care is palliative and directed to re-admission for COPD in the next 12 improving patients' experience of health and months (difference=4.8, 95% CI 1.6 to well being. 8.0). Patients who were re-admitted andStudies have found that QOL of patients died from COPD did not differ in SGRQ with COPD improves after intervention such scores from those who were re-admitted as taking part in pulmonary rehabilitation proand survived for more than 12 months. grammes. [8][9][10] However, improvement in QOL Re-admission was not related to sex, age, does not correlate very strongly with changes SGRQ subscales (Symptom, Impact and who used more acute serv...
Angiotensin II (ANG II) binds with high affinity to specific renal receptors and exerts major influences on hemodynamics and tubular transport. Glomerular and tubular epithelial receptors are well characterized in contrast to pre- and postglomerular and medullary vasculature. Therefore, the scope of this review is limited to an indepth comparison of ANG II receptor kinetics, analogue specificity, and mechanisms of receptor regulation and signal transduction in glomeruli and epithelial cells. Despite the fact that these receptors are in close proximity anatomically, there is evidence from a number of laboratories that permits classification into two distinct receptor subtypes. The receptor of the glomerular mesangium, classified herein as "type A," is characterized by high affinity for ANG II and the heptapeptide, des-Asp1-Ang II (ANG III), "downregulation" with high ambient concentrations of ANG II and signal transduction mediated by phospholipase C-induced Ca2+ transients. The tubular epithelial ANG II receptor, "type B," is of lower affinity for ANG II and ANG III, "upregulated" by high levels of ANG II and mediates inhibition of adenylate cyclase following coupling to an inhibitory GTP binding protein. Both receptors possess secondary mechanisms of signal transduction that may also participate in regulation of cellular function(s). These findings support the hypothesis that at least two distinct classes of ANG II receptors are present in the kidney cortex.
This study was carried out to investigate the relationship between induced sputum eosinophil apoptosis and clinical severity score, airway obstruction and symptom scores in patients with chronic stable asthma.Altogether, 41 chronic stable asthmatic subjects of varying severity defined by Aas score and 17 control subjects underwent spirometry, symptom questionnaire and successful sputum induction. Sputum was processed and cytospins prepared for light microscopy to determine normal and apoptotic eosinophils.Mild asthmatic subjects had a significantly lower percentage sputum eosinophils and a significantly higher eosinophil apoptotic ratio (AR) than moderate or chronic severe asthmatics. Severe asthmatic subjects had a significantly greater age, duration of asthma and sputum eosinophil count?mL -1 than mild asthmatic subjects. Asthmatic subjects9 symptom scores, severity scores and age inversely correlated with AR and the percentage of sputum eosinophils. Baseline forced expiratory volume in one second inversely correlated with percentage sputum eosinophils and positively correlated with AR.The study demonstrates a relationship between reduced sputum eosinophil apoptosis and increased clinical severity of chronic stable asthma, providing additional evidence that eosinophil apoptosis may be important in the resolution of eosinophilic airway inflammation in asthma. Eur Respir J 2003; 22: 484-490.
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