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At least 217 records · Page 12Linked to original sources
PubMed2004

Isoform-specific knockout of endothelial myosin light chain kinase: closing the gap on inflammatory lung disease.

Inflammatory lung diseases result in high rates of morbidity and mortality. Central to the pathogenesis of these diseases is disruption of endothelial barrier function. Activation of myosin light chain kinase (MLCK) is a key regulatory step in the modulation of endothelial permeability. Recent studies show that mice with selective knockout of the endothelial MLCK are less susceptible to endotoxin-induced acute lung injury and that a new small-molecule inhibitor of MLCK also protects against lung injury.

Animals↗
PubMed2006

Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs in the respiratory tract: potential implications in asthma and other lung diseases.

In healthy lung, Matrix Metalloproteinases (MMPs) and their physiological inhibitors, tissue inhibitors of matrix metalloproteinases (TIMPs), are produced in the respiratory tract by a panel of different structural cells. These activities are mandatory for many physiological processes including development, wound healing and cell trafficking. Deregulation of proteolytic-antiproteolytic network and inappropriate secretion of various MMPs by stimulated structural or inflammatory cells is thought to take part to pathophysiology of numerous lung diseases including asthma, chronic obstructive pulmonary disease (COPD), lung fibrosis and lung cancer. Cytokines and growth factors are involved in these inflammatory processes and some of those mediators interact directly with MMPs and TIMPs leading either to a regulation of their expression or changes in their biological activities by proteolytic cleavage. In turn, cytokines and growth factors modulate secretion of MMPs establishing a complex network of reciprocal interactions. Every MMP seem to play a rather specific role and some variations of their expression are observed in different lung diseases. The precise role of these enzymes and their inhibitors is now studied in depth as they could represent relevant therapeutic targets for many diseases. Indeed, MMP inhibition can lead either to a decrease of the intensity of a pathological process or, in the contrary for some of them, to an increase of disease severity. In this review, we focus on the role played by MMPs and TIMPs in asthma and we provide an overview of their potential roles in COPD, lung fibrosis and lung cancer, with a special emphasis on loops including MMPs and cytokines and growth factors relevant in these diseases.

Animals↗
PubMed2006

Gastro-oesophageal reflux and interstitial lung disease.

BACKGROUND: Interstitial lung disease is a heterogeneous entity, which encompasses a large number of pulmonary disorders, including idiopathic pulmonary fibrosis. Gastro-oesophageal reflux appears to be more prevalent in idiopathic pulmonary fibrosis than in controls and in patients with secondary pulmonary fibrosis, but its contribution to interstitial lung disease remains unsettled. AIMS: To prospectively evaluate gastro-oesophageal reflux in patients with interstitial lung disease and to define acid reflux patterns in patients with idiopathic and secondary forms of pulmonary fibrosis. MATERIALS AND METHODS: Twenty-eight patients (15M, median age 66 years, interquartile range 60-71) were studied by history taking, pulmonary function tests, high resolution computed tomography, oesophageal manometry and 24h oesophago-gastric pH monitoring. RESULTS: Sixteen patients (57%) had typical reflux symptoms. All patients completed 24h pH metry and 14 underwent oesophageal manometry. An abnormal oesophageal acid exposure was observed in 19 patients (68%), 13 of which complained of predominant typical reflux symptoms. A diagnosis of idiopathic pulmonary fibrosis was made in 18 patients, while the remaining 10 patients were classified as secondary pulmonary fibrosis. Secondary pulmonary fibrosis patients had more restrictive lung defect, as expressed as Tiffeneau index (p<0.05) and greater acid reflux at nighttime (p<0.05) than idiopathic pulmonary fibrosis patients. CONCLUSIONS: The prevalence of abnormal acid reflux in interstitial lung disease patients is high and, in particular, patients with secondary pulmonary fibrosis show higher oesophageal acid exposure than those with idiopathic form.

Aged↗
PubMed1998

Transcutaneous oxygen tension measurements during methacholine challenge of prematurity in infants with chronic lung disease.

Chronic lung disease (CLD) of prematurity may be caused by a number of insults during mechanical ventilation, including barotrauma and hyperoxia. To evaluate bronchial hyperresponsiveness (BHR) in infants with CLD of prematurity, we measured changes in transcutaneous oxygen tensions (tcPO2) during methacholine inhalation challenge. Twelve infants with CLD and 22 age-matched children without respiratory diseases were enrolled in this study (ages--5 to 36 months; mean age--16.2 months). Serial doses of methacholine were doubled until a 10% decrease in tcPO2 from baseline was reached. The cumulative dose of methacholine inhaled by the time tcPO2 had been reached (Dmin-PO2) was considered to represent the dose at which reactivity to methacholine (RO2meth) had occurred. In the CLD group, Dmin-PO2 (3.50 +/- 0.1 log x milli-units) was significantly lower than in the preterm control infant group (4.31 +/- 0.2 log x milli-units) and the term infant group (4.21 +/- 0.1 log x milli-units) (P = 0.004, P < 0.001). Dmin-PO2 in the preterm control infant group was not significantly different than in the term infant group (P > 0.5). These results suggest that infants who require additional therapeutic oxygen and mechanical ventilation during the early months of life are at risk of developing early-onset, long-lasting respiratory disease that is related to an acquired BHR.

Bronchial Hyperreactivity↗
PubMed1981

Physical therapy for children with chronic lung disease.

Chronic lung disease is a major health problem among children. Estimates suggest that one child in six has a chronic respiratory condition. This article reviews three common chronic respiratory conditions occurring in childhood for which physical therapy is usually recommended. The cause, pathophysiology, and medical treatment are explained for asthma, respiratory complications of chronic neuromuscular disease, and cystic fibrosis. The rationale for physical therapy and the concepts of treatment for the three disorders are presented. Major clinical studies that have attempted to document the efficacy of physical therapy are discussed. Questions for future research are proposed.

Asthma↗
PubMed1970

Regional lung function in patients with obstructive lung diseases.

Regional lung function was measured, using radioactive xenon-133, in a group of normal subjects and in three carefully defined groups of patients with obstructive lung disease. When compared with the normal subjects, patients in the emphysematous group showed a relative reduction of ventilation and perfusion to the upper zones, while patients having chronic bronchitis without cardiac or respiratory failure showed a predominantly lower zone defect. In the group of patients with chronic bronchitis with cardiac and respiratory failure no consistent pattern was found.

Aged↗
PubMed2005

Histone acetylation and deacetylation: importance in inflammatory lung diseases.

Inflammatory lung diseases are characterised by increased expression of multiple inflammatory genes that are regulated by proinflammatory transcription factors, such as nuclear factor-kappa B. Gene expression is regulated by acetylation of core histones through the action of coactivators, such as CREB-binding protein, with intrinsic histone acetyltransferase (HAT) activity. Conversely, gene repression is mediated via histone deacetylases (HDACs) and other corepressors. In asthma, there is an increase in HAT activity and some reduction in HDAC activity, which is restored by corticosteroid therapy. Corticosteroids switch off inflammatory genes in asthma through the inhibition of HAT activity and by the recruitment of HDAC2 to the activated inflammatory gene complex. In chronic obstructive pulmonary disease, there is a reduction in HDAC2 activity and expression, which may account for the amplified inflammation and resistance to the actions of corticosteroids. The reduction in HDAC2 may be secondary to oxidative and nitrative stress as a result of cigarette smoking and severe inflammation, and may also occur in severe asthma, smoking asthmatic patients and cystic fibrosis. Similar mechanisms may also account for the steroid resistance seen with latent adenovirus infections. The reduction in histone deacetylase activity can be restored by theophylline, which may be able to reverse steroid resistance in chronic obstructive pulmonary disease and other inflammatory diseases.

Acetylation↗
PubMed1993

Current issues in the assessment of interstitial lung disease.

Interstitial lung diseases (ILDs) are chronic disorders of the lower respiratory tract, characterized by inflammation and derangement of the alveolar walls. The major functional consequence is the loss of alveolar capillary units and, thus, a limitation of oxygen transfer from air to blood. In recent years, new insights into many aspects of alveolitis as the basic pathological substrate of these diseases, the different inflammatory and immune competent effector cells and their role in the mechanisms of injury and repair have changed our concepts about the pathogenesis of ILD. New techniques, such as bronchoalveolar lavage and computed tomography, allow a better assessment of disease activity and extent of the underlying process. This review also discusses the problems of classification of ILD, and concentrates on issues of assessment and markers of disease activity. Treatment is not a topic of this review but better assessment of these disorders is probably a prerequisite of further progress in treatment and prognosis.

Biomarkers↗
PubMed1997

[Estimation of 123I-metaiodobenzylguanidine lung uptake in heart and lung diseases--with reference to lung uptake ratio and decrease of lung uptake].

123I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy was performed in 64 patients with heart and lung diseases. Distribution of MIBG in the chest was evaluated by planar images, using counts ratios of the heart to the mediastinum (H/M) and the unilateral lung to the mediastinum (Lu/M). Most of patients with heart diseases showed obvious lung uptake of MIBG. The ratios of H/M were 1.75 +/- 0.20 in the group without heart failure and 1.55 +/- 0.19 in the group with heart failure. The ratios of Lu/M in the right and left lung were 1.56 +/- 0.16 and 1.28 +/- 0.16 in the group without heart failure. And those were 1.45 +/- 0.16 and 1.19 +/- 0.15 in the group with heart failure. But 3 patients complicated with chronic pulmonary emphysema and one patient with interstitial pneumonia due to dermatomyositis showed markedly decreased lung uptake. The ratios of Lu/M in the right and left lung of these patients were 1.20, 1.17; 1.17, 1.13; 1.01, 0.97 and 1.27, 0.94, respectively. These results suggest that the lung uptake of MIBG may reflect the state of pulmonary endothelial cell function in clinical situations, considering that it has been demonstrated that MIBG may be useful as a marker of pulmonary endothelial cell function in the isolated rat lung.

3-Iodobenzylguanidine↗
PubMed2003

[How are interstitial lung diseases diagnosed in Germany? Results of the scientific registry for the exploration of interstitial lung diseases ("Fibrosis registry") of the WATL].

From 1995 to 1999 we evaluated questionnaires sent by pulmonologists and departments of pulmonology in order to register interstitial lung diseases. On the whole 1142 patients (579 males, 563 females, mean age 51.1 +/- 15.3 years, sarcoidosis, n = 511, extrinsic allergic alveolitis, n = 145, idiopathic pulmonary fibrosis, n = 308, bronchiolitis obliterans organizing pneumonia (BOOP), n = 93, others, n = 85) were recorded in the registry. With reference to the mean age sarcoidosis occurred most frequently in the fourth decade and idiopathic pulmonary fibrosis in the sixth decade. In all these diseases bronchoscopy with bronchoalveolar lavage and transbronchial biopsy was predominantly used for further diagnosis. It was striking that high-resolution computed tomography of the thorax was still rarely used when diagnosing these diseases. Apart from the group with BOOP the number of non-smokers in men and women was decisively higher than the average of the population of Germany.

Biopsy↗
PubMed1974

Experimental immune complex disease of the lung. The pathogenesis of a laboratory model resembling certain human interstitial lung diseases.

Membranous and/or proliferative pneumonitis, similar in certain features to human interstitial pneumonitis, developed in rabbits making hyperactive antibody response to daily injections of bovine serum albumin (BSA) administered in multiple large doses sufficient to maintain the state of relative antigen-antibody equivalence. The pulmonary lesions were associated with deposition in alveolar capillary walls and interstitium of antigen, host globulin and complement, presumably in immune complexes. In some rabbits chronic interstitial pneumonitis, characterized by thickening of alveolar capillary walls, interstitial fibrosis and deposition of fibrinogen, was observed. The production of immune complex pneumonitis seems to depend on the degree of the antibody response because rabbits developing chronic serum sickness with low doses of BSA, rabbits with acute serum sickness as well as nonresponders showed no pulmonary alterations. This observation is comparable to that described by Dixon in his studies on experimental immune complex glomerulonephritis. It is conceivable that the pulmonary pathology shown here is produced by formation of larger amounts of complexes which may persist longer at critical levels in the circulation than in rabbits immunized with a single daily injection of BSA. In conclusion this study suggests: first, that experimental chronic serum sickness can be used as a model, not only for glomerulonephritis, but also for experimental systemic disease, comparable to human systemic diseases produced by circulating antigen-antibody complexes; and second, that the pathogenesis proposed here offers an alternative to using antilung basement membrane pneumonitis for the experimental approach to the study of human lung immunopathology.

Animals↗
PubMed2002

Clinical approach to chronic beryllium disease and other nonpneumoconiotic interstitial lung diseases.

Exposures in the workplace result in a diverse set of diseases ranging from the pneumoconiosis to other interstitial lung diseases to acute lung injury. Physician awareness of the potential disease manifestations associated with specific exposures is important in defining these diseases and in preventing additional disease. Most occupational diseases mimic other forms of lung disease, including pulmonary fibrosis, sarcoidosis, adult respiratory distress syndrome (ARDS), and bronchiolitis. A "sarcoidosis"-like syndrome, usually limited to the lungs, may result from exposure to bioaerosols and a number of metals. Exposure to beryllium in the workplace produces a granulomatous lung disease clinically indistinguishable from sarcoidosis, chronic beryllium disease (CBD). Beryllium's ability to produce a beryllium-specific immune response is used in the beryllium lymphocyte proliferation tests to confirm a diagnosis of CBD and exclude sarcoidosis. Exposure to other metals must also be considered in the differential diagnosis of sarcoidosis. When an individual presents acutely with ARDS or acute lung injury, an acute inhalational exposure must be considered. Exposure to a number of irritant substances at high levels may cause a "chemical pneumonitis" or acute lung injury, depending on the solubility and physicochemical properties of the substance. Some of the most notable agents include nitrogen and sulfur oxides, phosgene, and smoke breakdown products. Ingestion of paraquat may also result in an ARDS syndrome, with pulmonary fibrosis eventually resulting. Bronchiolitis is a rare manifestation of inhalational exposures but must also be considered in the clinical evaluation of inhalational exposure.

Adult↗