PubMed Health⌕ Search

Biomedical subjects

J Müller-Quernheim

Publications and source records attributed to J Müller-Quernheim.

131 records · Page 8Linked to original sources

Effect of sulfur dioxide on cytokine production of human alveolar macrophages in vitro.

Tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, and transforming growth factor-beta are cytokines synthesized by alveolar macrophages. We investigated the effect of sulfur dioxide, a major air pollutant, on the production of these cytokines by alveolar macrophages. The cells were layered on a polycarbonate membrane and exposed for 30 min to 0.0, 1.0, 2.5, and 5.0 ppm sulfur dioxide at 37 degrees C and 100% air humidity. The cells were incubated for 24 h after exposure, thus allowing cytokine release. Cytotoxic effects of sulfur dioxide were evaluated by trypan blue exclusion. Cytokines were measured with enzyme-linked immunosorbent assays (i.e., tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6) or by use of a specific bioassay (i.e., transforming growth factor-beta). The toxicity of sulfur dioxide for alveolar macrophages ranged from 3.1 % to 9.5 %. A 30-min exposure to sulfur dioxide induced a significant decrease in spontaneous and lipopolysaccharide-stimulated tumor necrosis factor-alpha (p < .001) and lipopolysaccharide-stimulated interleukin-1beta release (p < .05). The release of interleukin-6 and transforming growth factor-beta was not affected significantly by sulfur dioxide exposure. Our results demonstrated a functional impairment of alveolar macrophages after sulfur dioxide exposure (i.e., release of tumor necrosis factor-alpha and interleukin-1beta). Neither spontaneous nor stimulated release of interleukin-6 and transforming growth factors were influenced by exposure to sulfur dioxide.

Air Pollutants↗

Interstitial alveolitis as early manifestation of anti-Jo-1 positive polymyositis.

Polymyositis (PM), dermatomyositis (DM) and inclusion-body myositis belong to a heterogenous group of inflammatory myopathies. Pulmonary manifestations occur in a minority of PM patients due to infiltration of diaphragmatic and thoracic muscles or more rarely due to interstitial lung disease. Here, we report on the case of a 67-year-old patient who developed an interstitial idiopathic alveolitis as an early and rare manifestation of anti-Jo-1-positive polymyositis. Clinical and pathogenetical features of the PM associated interstitial alveolitis are discussed.

Aged↗

Regulation of cytokine release by alveolar macrophages treated with interleukin-4, interleukin-10, or transforming growth factor beta.

We evaluate the influence of IL-4, IL-10 and TGF-beta upon the release of IL-1 alpha, tumor necrosis factor-alpha (TNF-alpha), and IL-6 by lipopolisaccharide (LPS, 1 microgram/ml) stimulated alveolar macrophages (AM). IL-4 reduced TNF-alpha release, in a dose dependent manner, to 62% and IL-1 alpha release to 42% of LPS-stimulated AM without IL-4. IL-6 release was also suppressed (61%), however, with a biphasic dose response curve. IL-10 suppressed LPS induced release of IL-alpha and TNF-alpha to approximately 50% of control without affecting IL-6 release. When used at high concentrations, TGF-beta achieved moderate reductions of TNF-alpha and IL-1 alpha release. Low concentrations of LPS (0.1 microgram/ml), allowed a dose-dependent TGF-beta-induced suppression of TNF-alpha-release to approximately 80% of control. The combinations of IL-4 and IL-10 was more effective in suppressing IL-6 release, although the suppression was only weak. Other combinations of cytokines revealed no synergistic inhibitory activities. Our data demonstrate that IL-1 alpha and TNF-alpha release by AMs is down regulated by IL-4, IL-10, and TGF-beta. IL-6 release, however, can only be suppressed to some extent by a combination of IL-4 and IL-10.

Bronchoalveolar Lavage Fluid↗