Immunitat und Infektion最新文献

Extracellular matrix proteins are increased in inflammatory synovitis. We showed previously that the in situ expression of the corresponding extracellular matrix receptors (beta 1-integrins) is enhanced in synoviocytes (SC) of synovitis of different etiology (16). To investigate the adhesion of SC to extracellular matrix proteins, we examined the attachment of SC from normal and inflamed synovia to fibronectin, tenascin, laminin and collagen type IV. Compared to normal SC and SC of osteoarthritis, SC of rheumatoid arthritis showed an increased binding to tenascin, laminin, fibronectin and collagen type IV, suggesting a distinctive interaction of SC and extracellular matrix proteins in rheumatoid arthritis. Furthermore, the increased binding of SC of rheumatoid arthritis to extracellular matrix proteins may play a role in tissue remodelling associated with rheumatoid arthritis.

Resting, non-cycling mesangial cells (MCs) can be induced by IFN gamma to express the Fc gamma-RIIIa and Fc epsilon RI-gamma subunits of the CD16TM receptor complex. After cell surface expression of CD16TM by IFN gamma induction the binding of immune complexes to MCs induces IL-6 secretion. A Fc epsilon RI-gamma gene knockout has recently been described. It is now possible to study the function of Fc gamma RIIIa and other gamma chain associated Fc receptors in the initiation and progression of chronic glomerular inflammation in the context of the intact immune system in vivo.

The number of plasma cells, IgG+, IgA1+, IgA2+ and IgM+ cells were determined in bone marrow (BM) biopsies of 12 patients with common variable immunodeficiency syndrome (CVID) and 12 controls without signs of immunodeficiency. Controls had a median of 11 plasma cells/mm2, 76 IgG+, 76 IgA+ and 18 IgM+ cells/mm2 BM, respectively. Compared with the control group, the CVD patients showed a significant reduction of each cell type (p < 0.001). They also demonstrated a close correlation between low numbers of IgG+ and IgA+ cells in the BM and low IgG and IgA serum levels. In general, there was also a good correlation of the IgM+ cells and the respective IgM levels in the serum, except 2 CVID patients with normal IgM serum levels and subnormal numbers of IgM+ cells in the BM. Our results showed that there was an almost complete coincidence between the reduced numbers of Ig-producing cells in the BM and low serum levels of the respective Ig isotype. Thus, immunohistological analysis may be of additional help for the diagnosis of immunodeficiency.

Lipoprotein abnormalities are a risk factor for atherosclerotic disease and considered to accelerate glomerular injury in kidney disease. Serum levels of Lp(a) are elevated in patients with nephrotic syndrome and Lp(a) deposits are found in diseased glomeruli. Since mesangial hypercellularity is a prominent feature in a variety of glomerular diseases, we studied the effects of Lp(a) on proliferation of cultured rat mesangial cells. DNA synthesis was stimulated in cells incubated in the presence of Lp(a) as were the mRNA levels for c-fos and c-myc, two "early genes" that serve as transcription factors. Lp(a) also accelerated cell growth by 42 +/- 6% compared to control cells. Increased DNA synthesis was partially blunted, when cells were incubated with Lp(a) in the presence of oxygen radical scavengers CAT and SOD. We conclude that Lp(a) abnormalities are likely to contribute to glomerular injury in kidney disease. The mechanism by which Lp(a) alters the proliferation rate of mesangial cells involves the formation of reactive oxygen species.

The ubiquitous occurrence of Legionellae requires an exact typing of isolated strains in order to demonstrate the source of infection. Monoclonal antibodies, analysis of genomic and plasmid DNAs, and the typing of alloenzymes are suitable for this purpose. Typing of Legionella pneumophila serogroup 1 strains by using monoclonal antibodies was found to be a rapid and adequate method. Other serogroups of L. pneumophila and non-pneumophila species are of considerably less antigenic diversity, so that the use of monoclonal antibodies is not particular profitable. In such cases, genotypic methods are needed to discriminate between unrelated strains. There are no changes in the genome structure, defined as restriction patterns, during passages on artificial media and cultured Acanthamoeba. The possibility that different species, serogroups and monoclonal or genomic subtypes can be isolated in a given water supply points to necessity to test a sufficiently large number of colonies grown from the water samples. A clonal distribution of some Legionella strains has been observed.

Nosocomial infections with Staphylococcus aureus necessitate the prompt recognition of the infectious chain as well as a rapid investigation and exclusion of infectious sources. Conventional typification procedures (e.g. phage typing) and genotyping methods with pulsed-field gel electrophoresis (PFGE) are labor-intensive and time-consuming and can be performed only in a few laboratories. A new attractive typing technique for S. aureus utilizes the polymorphism of the coagulase (coa) gene as an epidemiological marker. This typing method is performed with primers, homologous to a conserved region within the coa gene, in order to amplify the sequences encoding the C-terminal region of this molecule. Since the number of repetitive sequences varies within the coa gene, the resulting PCR products of individual strains can be of different lengths. We have assessed the coa gene length polymorphism in 150 strains of S. aureus. By the sizes of the PCR products these strains could be categorized into 10 subgroups. AluI restriction analysis of the PCR products resulted in a significantly higher degree of discrimination. Since the repeated sequences, consisting of 81 base pairs, possess a high variability of the nucleotides, a characteristic restriction fragment length polymorphism (coa-RFLP) pattern is yielded. Overall, we could distinguish 64% of the clinical isolates by RFLP analysis; in strains sharing identical antibiograms, 56% could be distinguished. 46% oxacillin-resistant strains, some of which originated from epidemic outbreaks, could be discriminated by their RFLP pattern. Comparing these results with those obtained from the PFGE method, isolates which differed by their coagulase gene RFLP also differed by their PFGE patterns.(ABSTRACT TRUNCATED AT 250 WORDS)

In a 53-year-old female patient with recurrent, sometimes bloody diarrhea, the long standing diagnosis of an ANA-negative lupus erythematosus with membranoproliferative glomerulonephritis, leucocytoclastic vasculitis and chronic hepatitis was ruled out and the diagnosis of a hepatitis C associated cryoglobulinaemia was established. The origin of the diarrhea was due to intestinal vasculitis as a result of cold food or beverages.

Transmissible spongiform encephalopathies seem to contradict a dogma in microbiology. There is now increasing evidence that the infectious agents are proteins (prion proteins). These proteins seem to be able to catalyze conformational conversions of a host-encoded isoform. The altered conformation induces intracellular accumulation and may lead to polymerization into fibrils and amyloid rods. Catalytical interactions of infectious prion proteins and their cellular isoforms are dependent on the primary structure. These considerations may be helpful to evaluate the risk of transmission of BSE to humans.

The aim of the study was to investigate the frequency and clinical significance of anticardiolipin antibodies (aCL) in systemic lupus erythematosus (SLE). 32 of 100 patients with SLE had positive anticardiolipin antibodies. Increased aCL were associated with thrombosis, thrombocytopenia, miscarriage, vasculitic skin changes and neurological symptoms. The incidence of thrombosis, thrombocytopenia, and neurological symptoms was significantly increased in the aCL-positive group as compared to the aCL-negative group. These findings confirm the results of former investigations and underline the role of aCL in systemic lupus erythematosus.