European journal of respiratory diseases. Supplement最新文献

The aim of this study was to determine which precipitins against four antigens in 2,440 farmers are associated with the occurrence of farmer's lung (FL). The antigen panel consisted of mycelial antigens of Micropolyspora faeni, Thermoactinomyces vulgaris, Aspergillus fumigatus and Aspergillus umbrosus. As reference groups we used healthy farmers and those with chronic bronchitis. For the occurrence of precipitins against the four antigens there was a statistically significant difference between farmers with FL and healthy farmers but not between farmers with chronic bronchitis and healthy farmers. In a stepwise logistic linear regression analysis, farmers with FL and chronic bronchitis were compared to healthy farmers with respect to precipitins to the four antigens. Precipitins against Thermoactinomyces vulgaris differentiated farmers with FL (p less than 0.05) but not farmers with chronic bronchitis from healthy farmers. In Finland the occurrence of FL seems to be associated mainly with precipitins against Thermoactinomyces vulgaris, not with precipitins against Micropolyspora faeni as in Great Britain, and not with precipitins of Aspergillus umbrosus, which occurred most frequently in the sera of Finnish farmers. This association is in accordance with the exposure to spores of airborne moulds in farmers' work environment, where spore concentrations of Thermoactinomyces vulgaris have been measured to be about six times higher than those of Micropolyspora faeni.

One of the characteristic features of asthma is its tendency to become exacerbated during acute infections of the respiratory tract. There are only a few studies on the relation between infection and the exacerbation of asthma in adult asthmatics. Epithelial damage and airway inflammation, leading to transient increase in bronchial reactivity, are believed to be some of the mechanisms whereby respiratory infections cause asthmatic exacerbations. A total of 150 patients with asthma were studied. Study I, which dealt with the effect of respiratory infections on the exacerbation of asthma, comprised 92 asthmatics. The patients evaluated the severity of their disease daily by recording a symptom score in a follow-up chart. Peak expiratory flow (PEF) was measured by the patients with a mini-Wright peak flow meter twice a day. In order to detect respiratory infections, the occurrence of fever, sore throat and symptoms of rhinitis were also recorded. The daily self-observation by the patients was augmented by monthly examinations by a physician and an interview by a nurse. In the course of study I, 253 episodes of exacerbation of asthma were observed in 67 of the 92 patients. 63 (25%) of these 253 exacerbations were found in association with symptomatic respiratory infection (SRI). The mean duration of exacerbations associated with SRI was 11.4 days, significantly longer than the mean duration of 8.1 days of the other exacerbations. A series of 39 patients were entered in study II concerning the effect of vaccination on airway conductance and respiratory symptoms, and 27 asthmatics were assigned to study III which dealt with bronchial reactivity after vaccination with killed influenza virus vaccine. Study IV (bronchial reactivity after influenza A infection) comprised 13 patients. 21 members of hospital staff, without a history of chest disease, participated in studies II and IV as healthy controls. The virus vaccines in studies II, III and IV were provided by the manufacturers. The subjects were seen by the investigators immediately before and 2, 3 and either 14 or 21 days after vaccination. The presence of respiratory symptoms was assessed at each visit. In order to detect changes in respiratory function after vaccination, Raw and ITGV were measured at each visit. The results were expressed as specific airway conductance (SGaw). In studies III and IV, airway reactivity to inhaled histamine before and after vaccination was also measured.(ABSTRACT TRUNCATED AT 400 WORDS)

Lipids form a significant portion of airway mucus yet they have not received the same attention that epithelial glycoproteins have. We have analyzed, by thin layer chromatography, lipids present in airway mucus under "normal" and hypersecretory (pathological) conditions. The 'normals' included (1) bronchial lavage obtained from healthy human volunteers and from dogs and (2) secretions produced "in vitro" by human (bronchial) and canine (tracheal) explants. Hypersecretory mucus samples included (1) lavage from dogs made bronchitic by exposure to SO2, (2) bronchial aspirates from acute and chronic tracheostomy patients, (3) sputum from patients with cystic fibrosis and chronic bronchitis and (4) postmortem secretions from patients who died from sudden infant death syndrome (SIDS) or from status asthmaticus. Cholesterol was found to be the predominant lipid in 'normal' mucus with lesser amounts of phospholipids. No glycolipids were detected. In the hypersecretory mucus, in addition to neutral and phospholipids, glycolipids were present in appreciable amounts, often the predominant species, suggesting that these may be useful as markers of disease. Radioactive precursors 14C acetate and 14C palmitate were incorporated into lipids secreted "in vitro" by canine tracheal explants indicating that they are synthesised by the airway.

We studied the ultrastructure of superficial and deep samples of 40 resected primary lung carcinomas. Tumour cell differentiation was semiquantitatively assessed and differences between samples of a same tumour were evaluated. In two instances were major differences in ultrastructural diagnosis found between the samples of the same tumour. A further 9 cases showed one predominant differentiation in one sample, but two equally predominant differentiations in the second sample. The other 29 tumours did show occasional minor differences between the samples, but these differences did not result in differences in ultrastructural diagnosis.

Considerable advances have been made over the past 5 years of our understanding of the biology of lung tumours in particular SCLC. In this chapter, and in other sections of this symposium various aspects of these properties have been discussed. The greater understanding of the properties of these tumours should provide means whereby increased success can be achieved in clinical remissions and long term survival for the majority of patients with these diseases.

The airway surface mucosa begins in the naso-oro pharynx and lines the conducting airways, which include the trachea, major bronchi and bronchial divisions down to the level of the respiratory bronchioles. Although sampling methods used cannot completely isolate these specific areas, analysis of immunoglobulins shows variation especially in the relative proportions of secretory IgA, IgG and IgE. The air exchange surface is samples by bronchoalveolar lavage, principally, yielding alveolar secretions that contain IgG subclasses, surfactant, etc. and a variety of respiratory cells. Several diseases illustrate abnormalities that can occur in the availability of these immunoglobulins, or in their presumed antibody functions, contributing to human diseases that have a prominent component of infection. Secretory IgA either deficient or degraded by bacterial protease (especially IgA1 form) can reduce available anti-viral antibody or perhaps promote colonization of the airways with certain microbes. IgA has a dual role. As it is an important opsonic form of antibody, selective deficiency of IgG, especially subclasses IgG, and/or IgG4, can be associated with recurrent sinopulmonary infections. Sometimes IgG (IgG4) can be increased in hypersensitivity lung diseases including asthma and orga-antigen induced hypersensitivity pneumonitis (pigeon breeders disease). Finally, cystic fibrosis, affecting the lung with persistent infection often with Pseudomonas aeruginosa, can feature degradation of IgG antibody that may create blocking fragments that impair opsonin-induced phagocytosis, or this antibody can contribute to immune complex formation. Thus, immunoglobulins (antibodies) are an important ingredient of humoral host defenses in the respiratory tract and can contribute to disease, often involving infection, if quantitative or qualitative deficiencies in them exist.

The human tracheobronchial tree possesses several mechanisms for keeping itself clean and sterile. Mucociliary clearance results from the beating action of cilia lining the conducting airways and propelling the overlying mucus cephalad. Locally produced biological debris and inhaled, insoluble material are swept with the mucus and removed from healthy lungs within one day. Cough augments the often impaired mucociliary clearance of patients with excessive secretions. Cough is limited in is efficacy to the proximal airways. Energy transfer from airflow to mucus transport in airways lined with excessive secretions has been put forward as a third mechanism (two-phase gas-liquid flow) for the removal of lung secretions. Other mechanisms that have been proposed for clearance of lung secretions are: 'milking', 'squeezing' and peristalsis.