prostaglandin-d2 and Lung-Diseases

Topics: Anaphylaxis; Animals; Asthma; Bronchi; Dinoprost; Dinoprostone; Dogs; Epoprostenol; Guinea Pigs; Humans; In Vitro Techniques; Lung; Lung Diseases; Models, Biological; Muscle, Smooth; Prostaglandin D2; Prostaglandins; Prostaglandins D; Prostaglandins E; Prostaglandins F; SRS-A; Thromboxane A2

Topics: Anaphylaxis; Arachidonic Acid; Arachidonic Acids; Asthma; Basophils; Blood Platelets; Bronchial Provocation Tests; Calmodulin; Cyclic AMP; Deuterium; Deuterium Oxide; Histamine Release; Humans; Lung Diseases; Mast Cells; Peptide Hydrolases; Phospholipids; Platelet Activating Factor; Platelet Factor 4; Prostaglandin D2; Prostaglandins D; Receptors, IgE; Receptors, Immunologic; Serotonin; Water

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Aspirin; Asthma; Bronchitis; Dinoprost; Dinoprostone; Epoprostenol; Humans; Leukotriene B4; Lung; Lung Diseases; Prostaglandin D2; Prostaglandin Endoperoxides, Synthetic; Prostaglandin H2; Prostaglandins D; Prostaglandins E; Prostaglandins F; Prostaglandins G; Prostaglandins H; Pulmonary Circulation; Pulmonary Ventilation; SRS-A

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Aged; Alprostadil; Combined Modality Therapy; Cyclic AMP; Cyclic GMP; Dinoprost; Dinoprostone; Female; Humans; Laser Therapy; Lung Diseases; Male; Middle Aged; Pneumonectomy; Preoperative Care; Prostaglandin D2; Thoracoplasty; Thromboxane B2

Multiple factors contribute to the pathogenesis and prognosis of chronic obstructive pulmonary disease(COPD), still requiring new therapeutic strategies and medications for the disease. The aim of the present study is to investigate the model of lipopolysaccharide (LPS)-induced chronic lung injury and hyperinflation and test therapeutic effects of peroxisome proliferator-activated receptor (PPAR)-gamma agonist. Wister rats were challenged with intra-tracheal instillation of LPS at concentrations of 0.006, 0.060, 0.600, and 6.000 mg/ml per kg, twice a week, for 1, 2, 4 and 6 weeks. PPAR activator, 15-deoxy-Delta12,14-prostaglandin J2 (15D-PGJ2), or vehicle (PBS) was administered orally and daily at the dose of 1 and 10 mg/ml per kg in animals challenged with LPS or PBS at the dose of 0.060 mg/ml per kg body weight twice a week for 4 weeks. We found that intra-tracheal exposure of LPS resulted in a dose-dependent pattern of chronic lung hyperinflation and hypertrophy, increased alveolar enlargement, reduced vascular endothelial growth factor (VEGF) and elevated tissue inhibitor of metalloproteinases (TIMP)-1 levels in bronchoalveolar lavage (BAL) fluid, and early changes of leukocyte influx and interferon (IFN)-gamma levels in bronchoalveolar lavage (BAL) fluid. PPAR-gamma agonist ameliorated these changes related with the dose used.LPS-induced lung disease model shows some similarities with human disease, and PPAR-gamma agonist maybe an alternative for COPD therapy.

Topics: Animals; Bronchoalveolar Lavage Fluid; Female; Interferon-gamma; Leukocyte Count; Lipopolysaccharides; Lung; Lung Diseases; Lung Volume Measurements; Pneumonia; PPAR gamma; Prostaglandin D2; Pulmonary Alveoli; Pulmonary Disease, Chronic Obstructive; Pulmonary Emphysema; Rats; Rats, Wistar; Tissue Inhibitor of Metalloproteinase-1

A previous study has demonstrated that 15-deoxy-delta12,14-prostaglandin J2 (15d-PG J2) enhanced acute lung injury induced by lipopolysaccharide (LPS) in mice. The enhancement in acute lung injury by 15d-PG J2 was concomitant with the enhanced expression of interleukin-1beta and chemokines in the lung. However, other underlying mechanisms of this enhancement remain to be elucidated. Cyclooxygenase (COX)-2 has been reported to be involved in enhanced pulmonary permeability during acute lung injury. This study investigated the effects of 15d-PG J2 on COXs expressions in the lung in the presence or absence of LPS. ICR mice were divided into 4 experimental groups that intratracheally received vehicle, lipopolysaccharide (LPS: 125 microg/kg), 15d-PG J2 (1 mg/kg), or 15d-PG J2 + LPS. The expression of mRNA for both COX-1 and -2 in the lung was evaluated 4 h after the intratracheal administration. 15d-PG J2 enhanced the COX-2 mRNA expression in the presence of LPS. In contrast, 15d-PG J2 did not affect the COX-1 expression. These results suggest that the enhancing effects of 15d-PG J2 on LPS-induced acute lung injury might be explained, at least in part, by those on the lung expression of COX-2.

Topics: Animals; Bacterial Toxins; Cyclooxygenase 1; Cyclooxygenase 2; Enterotoxins; Escherichia coli Proteins; Isoenzymes; Lipopolysaccharides; Lung; Lung Diseases; Male; Membrane Proteins; Mice; Mice, Inbred ICR; Prostaglandin D2; Prostaglandin-Endoperoxide Synthases; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger

We evaluated the levels of bradykinin, albumin, TAME-esterase activity, histamine, PGD2 and LTC4 in bronchoalveolar lavage fluid from asthmatics and from patients with pneumonia, sarcoidosis, fibrosis, and chronic bronchitis. Compared with the results of healthy volunteers and atopic asymptomatic asthmatics the bradykinin levels and TAME-esterase activity were significantly elevated. In all other groups, histamine was additionally elevated in asymptomatic asthmatics, whereas albumin was elevated in symptomatic asthmatics and fibrosis patients, and decreased in chronic bronchitis and pneumonia patients. Following local intrabronchial allergen challenge of mild grass pollen asthmatics out of season bradykinin levels increased significantly, correlated with albumin, histamine and TAME-esterase activity. In contrast to the increased mediator concentrations in the early phase reaction there was no change of BAL cells in asthmatics compared to baseline and healthy volunteers. The presence of bradykinin in the bronchoalveolar space of patients with active pulmonary inflammations and bradykinin generation in asthmatics as a result of intrabronchial allergen challenge provides strong evidence that kinins are involved in inflammatory disorders of the lower airways.

Topics: Asthma; Bradykinin; Bronchoalveolar Lavage Fluid; Histamine; Humans; Inflammation; Lung Diseases; Peptide Hydrolases; Prostaglandin D2; Reference Values; Serum Albumin; SRS-A