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Biomedical subjects

T Vischer

Publications and source records attributed to T Vischer.

11 recordsLinked to original sources
PubMed1995

Lipopolysaccharide binding protein as a marker of inflammation in synovial fluid of patients with arthritis: correlation with interleukin 6 and C-reactive protein.

OBJECTIVE: To determine levels of lipopolysaccharide binding protein (LBP) in serum and in synovial fluid (SF) of patients presenting with various articular disorders [degenerative arthritis, rheumatoid arthritis (RA), reactive arthritis (ReA)] and to correlate these levels with C-reactive protein (CRP) and interleukin 6 (IL-6), 2 markers of the acute phase response. METHODS: LBP was measured by a radioimmunoassay made up of lipopolysaccharide (LPS) to capture LBP and radiolabelled anti-LBP antibodies to detect LBP. LBP was also measured for its ability to present fluorescein isothiocyanate LPS (FITC-LPS) to human monocytes. CRP was measured by nephelometry and IL-6 bioassay. RESULTS: Levels of LBP in serum and in SF were significantly higher in patients with RA and ReA than in the control group of degenerative arthropathies. In the latter group, LBP values were similar to those found in controls. Serum LBP values correlated positively with SF LBP values. LBP values also correlated with CRP and IL-6 levels measured in SF. Functionally, LBP was found to be active and able to present LPS to monocytes, resulting in tumor necrosis factor-alpha (TNF-alpha) release upon LPS challenge. CONCLUSION: These in vitro data support the observation that LBP could play a major role in local joint disorders. Our results also strengthen the view that LBP may be a new marker of synovial inflammation.

Acute-Phase Proteins↗
PubMed1992

Inhibitors of interleukin 1 activity in synovial fluids and in cultured synovial fluid mononuclear cells.

Measurement of interleukin 1 (IL-1) in synovial fluids (SF) yielded variable results and implied the presence of an inhibitory activity. As peripheral blood monocytes produce an IL-1 receptor antagonist (IL-1ra), we investigated whether SF mononuclear cells (SFMC) also secreted such inhibitory activity. MC isolated from inflammatory SF produced, in addition to variable levels of IL-1, a specific IL-1 inhibitor of approximately 23 kDa which blocked both IL-1 biological activity and binding to its receptor. Western blot, using a polyclonal antibody to rhIL-1ra, indicated that SFMC secreted material that shared immunological crossreactivity with the cloned IL-1ra. IL-1 inhibitory activity was also detected in SF but not formally demonstrated to be related to IL-1ra. In conclusion, SFMC could produce IL-1ra and an imbalance between IL-1 and its specific antagonist may be relevant to the severity of joint destruction.

Blotting, Western↗
PubMed1989

Molecular interactions of Leishmania promastigote surface protease with human alpha 2-macroglobulin.

The interaction of Leishmania promastigote surface protease (PSP) with the plasmatic protease inhibitor alpha 2-macroglobulin (alpha 2M) was investigated. In plasma, solubilized PSP forms covalent complexes only with alpha 2M, at the exclusion of other protease inhibitors. The formation of complexes is accompanied by the proteolytic cleavage of the alpha 2M subunit and by the transition from the 'slow' to the 'fast' form of alpha 2M. The proteolytic activity of solubilized PSP on azocasein is inhibited by alpha 2M. In contrast, we found no evidence for a specific interaction of alpha 2M with the surface of promastigotes and PSP proteolytic activity on intact cells was not inhibited by alpha 2M.

Animals↗
PubMed1965

Homologous disease in the adult rat, a model for autoimmune disease. II. Findings in the joints, heart, and other tissues.

Polyarthritis and cardiac lesions have been observed in the adult rat with homologous disease. Changes in the lymphoid tissue and kidney have also been noted. A migratory polyarthritis occurred in over half of the affected animals, and cardiac involvement of varying intensity was present in all. Histologically, the arthritis was characterized by a mononuclear synovial inflammatory reaction. In the heart, the valves and myocardium demonstrated a similar type of response. Cultures of involved joints and hearts for pyogens and pleuropneumonia-like organisms were negative. The lymphoid tissues showed progressive changes in three stages: (a) disappearance of follicles; (b) increase in plasma-like cells and histiocytes; and (c) fibrosis. The second stage tended to coincide with the development of the polyarthritis. The kidney showed mild interstitial mononuclear infiltration. The pathologic changes described appear to be a consequence of reaction between foreign immunologically competent cells and host antigens, but the possibility that these lesions represent a response to antigens derived from unknown infectious agents is, however, not ruled out.

Animals↗