Plasma exudation in the airways: mechanisms and function

Persson, C. G. A.

doi:10.1183/09031936.93.04101268

Cited by 44 publications

(1 citation statement)

References 18 publications

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“…These data have led to the current hypothesis that T-lymphocyte subsets, mast cells and/or basophils activate eosinophils through the release of cytokines, such as interleukin-5 (IL-5) [4,21,22], subsequently producing the characteristic pathological abnormalities in asthma [3,4,12]. Hyperresponsiveness then develops as a result of increased inflammatory mediator release [23,24], inflammatory swelling of the airway wall [25], caused by plasma exudation [26] and/ or smooth muscle hypertrophy or hyperplasia [27). Furthermore, hyperresponsiveness might be enhanced by increased thickness of the subepithelial collagen layer [28).…”

Section: Asthma and Airway Hyperrespoosivenessmentioning

confidence: 99%

Virus-induced airway hyperresponsiveness in man

Sterk¹

1993

Eur Respir J

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Airway hyperresponsiveness is the most prominent functional abnormality in asthma. Although its aetiology is still unclear, it is well-known that allergen exposure and virus infections can temporarily induce or aggravate airway hyperresponsiveness. Among these environmental factors, virus infections appear to be clinically most relevant, since recent epidemiological studies have shown that most asthma exacerbations in children are associated with positive nasopharyngeal viral identification. The pathogenesis of virus-induced airway hyperresponsiveness has been investigated by experimental virus infections in animals and in man. Intranasal inoculation and/or inhalation of live attenuated influenza virus, or certain strains of rhinovirus, have been shown to induce airway hyperresponsiveness to various bronchoconstrictor stimuli in man. This indicates that experimental virus-infection, like allergen challenge, is an appropriate investigational model of asthma. The mechanisms of virus-induced airway hyperresponsiveness are still unclear, but may, in part, be similar to those involved in the pathogenesis of asthma. Currently investigated hypothesis include: epithelial damage or dysfunction, immunological responses, inflammatory mediator release, cholinergic and/or noncholinergic reflexes, and impaired beta-adrenoceptor function. Careful experimental studies, using modern laboratory techniques, are needed to unravel the role of viruses in the development of airway hyperresponsiveness. The results of such studies can potentially lead to an improvement of future asthma management.

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Section: Asthma and Airway Hyperrespoosivenessmentioning

confidence: 99%

Virus-induced airway hyperresponsiveness in man

Sterk¹

1993

Eur Respir J

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BPI‐ANCA of pediatric cystic fibrosis patients can impair BPI‐mediated killing of E. coli DH5α in vitro

Schultz

Schinke

Mosler

et al. 2004

Pediatric Pulmonology

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Gram-negative bacterial lung infections and chronic bacterial colonization are major threats for pediatric cystic fibrosis (CF) patients. Besides impeded mucociliary clearance, other mechanisms that contribute to increased susceptibility to infections are presumed. The bactericidal/permeability-increasing protein (BPI), which is delivered by neutrophil granulocytes and mucosal epithelial cells, is one of the most potent innate antibiotics against Gram-negative bacteria and endotoxin. Antineutrophil cytoplasmic autoantibodies against BPI (BPI-ANCA) have been found in up to 90% of CF patients, and titers correlated inversely with lung function parameters. As major pulmonary damage is mediated by Gram-negative bacteria and their products, the question was raised as to whether BPI-ANCA can inhibit the antibiotic function of BPI in these patients. Sera of 23 pediatric CF patients were analyzed for the presence of BPI-ANCA by indirect immunofluorescence, ELISA, epitope mapping, and Western blotting. Patients' IgG were tested in a bacterial growth inhibition assay with recombinant BPI (rBPI) and an amino-terminal fragment of BPI (rBPI(21)) that retains antibiotic activity for inhibition of the antibiotic function of BPI against E. coli DH5alpha in vitro. BPI was recognized by 21 of 23 patients' sera in our detection assays. Thirteen of 23 patients' BPI-ANCA (56%) could inhibit the antibiotic function in vitro. Moreover, epitope mapping over the whole BPI sequence revealed that more patients' BPI-ANCA recognize the amino-terminal part of BPI than can be detected by ELISA. Thus, in pediatric CF patients, BPI-ANCA may contribute to diminished bacterial clearance by inhibiting the antibiotic function of BPI.

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Can bronchodilator response predict bronchial response to methacholine in preschool coughers?

Beydon

Mbuila

Peiffer

et al. 2008

Pediatric Pulmonology

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The aim of the present study was to determine the relationship between bronchodilator response, assessed by interrupter resistance (Rint), and bronchial reactivity in preschool children with chronic cough. Thirty-eight children coughers (median age 5.0 years, range 2.8-6.4) were tested. Bronchodilator response was recorded within 4 months before methacholine challenge. Response to the latter was assessed using transcutaneous partial pressure of oxygen and Rint. Children were considered responders if a 20% fall in transcutaneous partial pressure of oxygen occurred during the bronchial challenge. Bronchodilator response was not different between responders (n = 24) and nonresponders (n = 14) [median (range) -0.11 (-0.44-0.09) vs. -0.08 (-0.21-0.10) kPa L(-1) sec; respectively]. However, none of the nonresponders had a bronchodilator response larger than -0.21 kPa L(-1) sec, this cutoff had a 100% positive and a 44% negative predictive value to predict a positive methacholine challenge. The relationship between bronchodilator response and bronchial methacholine responsiveness reached the limit of significance (P = 0.048). Furthermore, the magnitude of the bronchodilator response was correlated to the level of methacholine-induced level of bronchoconstriction (P = 0.01), and to the postchallenge bronchodilation (P = 0.04), all values expressed as % predicted. Moreover, the postbronchodilator Rint value obtained with preceding methacholine challenge was lower than the postbronchodilator value without preceding methacholine challenge in 71.4% (10/14) of the nonresponders and in only 33.3% (8/24) of the responders. Conclusions in preschool coughers bronchodilator response, assessed by the interrupter technique, was correlated to the bronchial responsiveness to methacholine. Non responders had a bronchodilator response not larger than -0.21 kPa L(-1) sec.

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Plasma exudation in the airways: mechanisms and function

Cited by 44 publications

References 18 publications

Virus-induced airway hyperresponsiveness in man

Virus-induced airway hyperresponsiveness in man

BPI‐ANCA of pediatric cystic fibrosis patients can impair BPI‐mediated killing of E. coli DH5α in vitro

Can bronchodilator response predict bronchial response to methacholine in preschool coughers?

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