Interleukin 10 Inhibits Alveolar Macrophage Production of Inflammatory Mediators Involved in Adult Respiratory Distress Syndrome
| Autor: | H. Gill Cryer, Chong-Jeh Lo, Minjuan Fu |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Lipopolysaccharides
Male Lipopolysaccharide medicine.medical_treatment Pharmacology Lung injury Proinflammatory cytokine chemistry.chemical_compound Macrophages Alveolar Animals Humans Medicine Protein Kinase C Protein kinase C Respiratory Distress Syndrome Newborn Tumor Necrosis Factor-alpha business.industry Osmolar Concentration Infant Newborn Intracellular Membranes Blood Coagulation Factors Interleukin-10 Enzyme Activation Interleukin 10 Cytokine chemistry Immunology Alveolar macrophage Calcium Surgery Tumor necrosis factor alpha Rabbits Inflammation Mediators business |
| Zdroj: | Journal of Surgical Research. 79:179-184 |
| ISSN: | 0022-4804 |
| DOI: | 10.1006/jsre.1998.5418 |
| Popis: | Background. Adult respiratory distress syndrome (ARDS) causes severe morbidity and mortality in trauma patients. One potential method to attenuate the lung injury is to inhibit alveolar macrophage production of proinflammatory mediators. The purpose of this study was to investigate the cellular mechanism of interleukin 10 (IL-10) inhibition on LPS-stimulated macrophage (Mφ). We hypothesized that IL-10 inhibited phospholipase C signal pathways in Mφ. IL-10 inhibition would be restored by calcium ionophores and protein kinase C (PKC) activation. Methods. Rabbit alveolar Mφ were obtained by bronchoalveolar lavage. Mφ were treated with Escherichia coli LPS (10 ng/ml) in the presence of various concentrations of human IL-10. Cell lysates and supernatant were analyzed for proagulants (PCA) and tumor necrosis factor (TNF), respectively. TNF mRNA expression of alveolar Mφ was also measured by Northern Blot assay. Macrophage PGE 2 production was measured by ELISA. Results. IL-10 inhibited the production of both TNF and PCA by LPS-stimulated Mφ. In addition, IL-10 also reduced TNF mRNA expression. Similarly, PGE 2 production by LPS-stimulated Mφ was also attenuated by IL-10. An increase in the intracellular [Ca 2+ ] induced by A23187 failed to reverse this IL-10-mediated inhibition. In comparison, phorbol myristate acetate, a protein kinase C (PKC) activator, restored TNF and PCA production despite the presence of IL-10. Conclusions. IL-10 inhibits Mφ production of inflammatory mediators. This inhibition is, at least in part, mediated by modulating the PKC activity. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect