Background: Alveolar macrophages (AM) are known to play an important role in the regulation of inflammatory reactions in the lung, e.g. during the development of chronic lung diseases.
View Article and Find Full Text PDFProduction of superoxide radicals is a central property of professional phagocytes used to combat invading microorganisms. Even though the number of macrophages and neutrophils is often increased in the lungs of patients with chronic lung diseases, these patients frequently suffer from bacterially induced exacerbations. To understand the underlying mechanisms, we investigated the production of superoxide radicals by bronchoalveolar lavage (BAL) cells in a rat NO(2) exposure model (10 ppm NO(2) for 1, 3, or 20 days).
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
March 2003
Inflammatory mechanisms are thought to play an important role in the pathogenesis of acute and chronic obstructive pulmonary diseases. In a rat inhalation model using continuous exposure to 10 ppm nitrogen dioxide for 1, 3, and 20 d, we investigated the inflammatory response with particular focus on the activation state of alveolar macrophages. Whereas the number of inflammatory cells and total protein concentration were increased in the bronchoalveolar lavage (BAL), the amount of the proinflammatory cytokine tumor necrosis factor-alpha was markedly reduced with increasing exposure time.
View Article and Find Full Text PDFRecently, a number of interleukin-10 (IL-10) homologues, among them IL-24 formerly known as melanocyte differentiation factor-7 (mda-7), has been described. Since IL-10 is released by macrophages and plays an important role in the resolution of inflammatory processes, we hypothesized that IL-24 might also be expressed in cells of the monocyte/macrophage lineage. We analyzed IL-24 expression on the mRNA and protein level in stimulated rat and human macrophages.
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