IL-17-producing T Lymphocytes in Lung Tissue and in the Bronchoalveolar Space after Exposure to Endotoxin from Escherichia coli in vivo – Effects of Anti-Inflammatory Pharmacotherapy
Résumé
Interleukin (IL)-17 may play a critical role for the innate immune response in mammals. However, little is known about its production in T-lymphocytes bronchoalveolar of anti-inflammatory pharmacotherapy on this IL-17 production. exposure to endotoxin from Escherichia Coli increases extracellular IL-17 protein in samples during 3 days, and is accompanied by a local increase in neutrophils and other inflammatory cells. This endotoxin exposure elevates IL-17 mRNA in lung tissue samples. after endotoxin exposure, the absolute number of CD3-positive cells containing intracellular IL-17 protein is increased as well; from a moderate cell number in lung tissue samples and from virtually none in BAL samples; with the number in lung tissue exceeding that observed in BAL samples. A high systemic dose of a glucocorticoid receptor agonist attenuates the endotoxin-induced increase in extracellular IL-17 protein in BAL samples, IL-17 mRNA in lung tissue samples, and in IL-17-containing CD3-positive cells in BAL and lung tissue samples. This is also true for the endotoxin-induced accumulation of neutrophils and other inflammatory BAL cells . exerts a less complete and more selective effect on the endotoxin-induced increase in extracellular IL-17 protein and on neutrophils in BAL samples. In conclusion, endotoxin-induced IL-17 production and release from T lymphocytes originates from cells that reside in lung tissue and from cells that The sustained IL-17 production and the associated neutrophil accumulation may be inhibited non-selectively through glucocorticoid receptor stimulation and more selectively through calcineurin phosphatase inhibition.
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