dinoprost has been researched along with Pulmonary-Eosinophilia* in 2 studies
2 other study(ies) available for dinoprost and Pulmonary-Eosinophilia
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Maternal exposure to combustion generated PM inhibits pulmonary Th1 maturation and concomitantly enhances postnatal asthma development in offspring.
Epidemiological studies suggest that maternal exposure to environmental hazards, such as particulate matter, is associated with increased incidence of asthma in childhood. We hypothesized that maternal exposure to combustion derived ultrafine particles containing persistent free radicals (MCP230) disrupts the development of the infant immune system and results in aberrant immune responses to allergens and enhances asthma severity.. Pregnant C57/BL6 mice received MCP230 or saline by oropharyngeal aspiration on gestational days 10 and 17. Three days after the second administration, blood was collected from MCP230 or saline treated dams and 8-isoprostanes in the serum were measured to assess maternal oxidative stress. Pulmonary T cell populations were assayed in the infant mice at six days, three and six weeks of postnatal age. When the infant mice matured to adults (i.e. six weeks of age), an asthma model was established with ovalbumin (OVA). Airway inflammation, mucus production and airway hyperresponsiveness were then examined.. Maternal exposure to MCP230 induced systemic oxidative stress. The development of pulmonary T helper (Th1/Th2/Th17) and T regulatory (Treg) cells were inhibited in the infant offspring from MCP230-exposed dams. As the offspring matured, the development of Th2 and Treg cells recovered and eventually became equivalent to that of offspring from non-exposed dams. However, Th1 and Th17 cells remained attenuated through 6 weeks of age. Following OVA sensitization and challenge, mice from MCP230-exposed dams exhibited greater airway hyperresponsiveness, eosinophilia and pulmonary Th2 responses compared to offspring from non-exposed dams.. Our data suggest that maternal exposure to MCP230 enhances postnatal asthma development in mice, which might be related to the inhibition of pulmonary Th1 maturation and systemic oxidative stress in the dams. Topics: Age Factors; Animals; Asthma; Bronchial Hyperreactivity; Cytokines; Dinoprost; Female; Gestational Age; Inflammation Mediators; Inhalation Exposure; Lung; Maternal Exposure; Mice, Inbred C57BL; Ovalbumin; Oxidative Stress; Particulate Matter; Pregnancy; Prenatal Exposure Delayed Effects; Pulmonary Eosinophilia; Severity of Illness Index; T-Lymphocytes, Regulatory; Th1 Cells; Th17 Cells; Th2 Cells | 2013 |
PGE2 and PGF2 alpha content in bronchoalveolar lavage fluid obtained from patients with eosinophilic pneumonia.
Cell differential, prostaglandins (PGs) E2 and F2 alpha in the bronchoalveolar lavage fluid (BALF) in two patients with eosinophilic pneumonia were measured at different times in the course of the disease. Results showed markedly increased numbers of eosinophils and increased content of prostaglandin (PG) E2 in BALF obtained from the patients with eosinophilic pneumonia compared to that of normal volunteers. Interestingly, the increased content of PGE2 in BALF obtained from the patients reverted to normal range with corticosteroid treatment. This change in PGE2 content in BALF was accompanied by normalization of number and percentage of eosinophils in BALF. These findings indicated that PGE2 level in lower respiratory tract of patients with eosinophilic pneumonia may be related to an increased number of eosinophils. Topics: Adult; Bronchi; Dinoprost; Dinoprostone; Eosinophils; Female; Humans; Leukocyte Count; Male; Middle Aged; Prednisolone; Prostaglandins E; Prostaglandins F; Pulmonary Eosinophilia; Therapeutic Irrigation | 1987 |