No abstract available.
Lymphangioma, Cystic*

BACKGROUND: PM is known to induce various pulmonary diseases, including asthma, cancer, fibrosis and chronic bronchitis. Despite the epidemiological evidence the pathogenesis of PM-related pulmonary diseases is unclear. METHODS: This study examined the effects of PM exposure on the secretion of TNF-alpha and IL-1beta in the cultured alveolar macrophages. The cultured primary alveolar macrophages were treated with the medium, PM (5~20 microgram/cm2), LPS (5ng/ml), and PM with LPS for 24h and 48h respectively. ELISA was used to assay the secreted TNF-alpha and IL-beta in the culture medium. Western blotting was used to identify and determine the level of proteins isolated from the culture cells. The cells cultured in the Lab-Tek(R) chamber slides were stained with immunocytochemical stains. RESULTS: PM induced TNF-alpha and IL-1beta secretion in the culturing alveolar macrophages, collected from the SPF and inflammatory rats. However, the effects were only dose-dependent in the inflammatory macrophages. When the cells were co-treated with PM and LPS, there was a significant synergistic effect compared with the LPS in the both cell types. CONCLUSION: PM might be play an important role in the induction and/or potentiation of various lung diseases by oversecretion of TNF-alpha and IL-1beta.
Animals ; Asthma ; Blotting, Western ; Bronchitis, Chronic ; Coloring Agents ; Enzyme-Linked Immunosorbent Assay ; Fibrosis ; Lung Diseases ; Macrophages ; Macrophages, Alveolar* ; Rats ; Tumor Necrosis Factor-alpha*

BACKGROUND: Particulate matters (PM) when inhaled is known to induce pulmonary diseases including asthma and chronic bronchitis when inhaled. Despite the epidemiological proofevidence, the pathogenesis of PM-related pulmonary diseases is unclearremain poorly understood. METHODS: Primary alveolar macrophages were harvested from the SPF and inflammatory rats by bronchioalveolar lavage (BAL). The cultured primary alveolar macrophages were treated with the medium only, PM only (5~40 microgram/cm2), LPS (5ng/ml) only, and PM with LPS for 24 and 48 hours. The level of secreted nitric oxide (NO) was assayed from the cultured medium by using the Griess reaction. The cultured cells were utilized for the western blotting against the inducible nitric oxide synthase (iNOS) proteins. Immunocyto- chemical staining against the iNOS and NT-proteins were performed in cells that cultured in the Lab-Tek(R) chamber slide after treatments. RESULTS: The PM that utilizein this experiments induced NO formation with iNOS expression in the cultured SPF and inflammatory rats alveolar macrophages, by itself. When the cells were co-treated with PM and LPS, there was a statistically significant synergistic effect on NO formation and iNOS expression over the LPS effect. The cells from the sham control showed minimal immunoreactivity for the NT-proteins. Significantly higher quantities of NT-proteins were detected in the PM and PM with LPS co-treated cells than from the sham control. CONCLUSION: Increased iNOS expression and NO formation with increased NT-proteins formation might be involved in the pathogenesis of PM-induced lung injury.
Animals ; Asthma ; Blotting, Western ; Bronchitis, Chronic ; Bronchoalveolar Lavage ; Cells, Cultured ; Lung Diseases ; Lung Injury ; Macrophages, Alveolar* ; Nitric Oxide Synthase Type II ; Nitric Oxide* ; Rats