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Biomedical subjects

J Heesemann

Publications and source records attributed to J Heesemann.

At least 199 records · Page 11Linked to original sources
PubMed1991

Evasion of Yersinia enterocolitica serotype 03 from complement-mediated killing.

Using isogenic strains of Y. enterocolitica serotype 03 (isolate 75) differing in LPS side chains (S and R), plasmid content (p+ and p-) or selective failure of YOP1 expression (YOP1-) we observed comparable C9 consumption via the alternative pathway by all strains. Differences became apparent in the bactericidal assays in which the 75S p+ strain was resistant whereas the plasmid-negative S and R strains were killed. Increased but submaximal resistance was observed with the 75R p+ and 75S YOP1- strains indicating that LPS side chains and plasmid-encoded factors other than YOP1 also contribute to serum resistance. Deposition of C9 and terminal complement complex (TCC) formation were greatly reduced on the resistant 75S p+ strain compared to the sensitive 75S p- strain. The 75S YOP1- variant behaved like the 75S p- strain with respect to C9 deposition and TCC formation suggesting that YOP1 prevents terminal C activation. A comparison of TCC deposited on resistant and sensitive Y. enterocolitica revealed no differences with respect to their salt- and protease-resistance and their size. We conclude from our experiments that serum resistance of 75S p+ depends on several surface components YOP1 being the most important. The YOP1 protein clearly interferes with C9 deposition and TCC formation and thereby contributes to serum resistance of plasmid-positive, YOP1 expressing Y. enterocolitica.

Centrifugation, Density Gradient↗
PubMed1990

[Yersinia-induced arthritis: new knowledge of pathogenesis, diagnosis and therapy].

Yersinia infections have been identified in rising incidence as the cause of acute or subacute intestinal or extraintestinal diseases in the past two decades. Immunopathological manifestations of Yersinia infections, e.g. Yersinia-induced arthritis, have evoked special interest among clinicians and microbiologists. Beneath epidemiological and clinical characteristics this review focuses on recent progress in pathogenesis and serological and immunohistological diagnosis of Yersiniosis. Possible consequences for newly therapeutical approaches in chronic Yersinia-induced arthritis and spondarthritis were discussed.

Antibodies, Bacterial↗
PubMed1990

Yersinia enterocolitica in the synovial membrane of patients with Yersinia-induced arthritis.

Using a monospecific rabbit antibody against Yersinia enterocolitica outer membrane protein 1, we examined synovial biopsy specimens from 7 patients with Yersinia-induced arthritis. Yersinia were demonstrated in the synovial membrane by indirect immunofluorescence in 4 patients with Yersinia-induced arthritis, but not in 6 control patients with Salmonella-induced arthritis or with rheumatoid arthritis. These findings suggest the persistence of Yersinia in the joints of patients with Yersinia-induced arthritis.

Adult↗
PubMed1990

Antibody activity against lipopolysaccharides, lipid A and proteins from Enterobacteriaceae in patients with chronic inflammatory liver diseases.

These studies are concerned with detection of circulating antibodies against various defined enterobacterial antigens in patients with chronic inflammatory liver diseases such as chronic hepatitis type B (n = 46), chronic active hepatitis (CAH) of autoimmune type (n = 10), alcoholic cirrhosis (n = 24) and primary biliary cirrhosis (PBC) (n = 24) as well as in healthy individuals (n = 39). Anti-LPS and anti-lipid A were determined by hemolytic and hemagglutination assay. Immunoblot technique was used to investigate the antibody activity against plasmid encoded proteins from Yersinia enterocolitica. Persistent titers of anti-LPS up to serum dilution 1:32.768 were found with hemolytic and hemagglutination assay in patients with alcoholic cirrhosis or PBC and in healthy control. In contrast nearly 50% of patients with chronic hepatitis B had no hemolytic antibodies against the two LPS E. coli serotypes at the time of liver biopsy. Anti-lipid A was detectable in 58% of patients with alcoholic cirrhosis but in low titers in less than 10% in the other groups (p less than 0.001). Alcoholic cirrhosis was also associated with a high frequency of IgG and IgA antibodies against plasmid encoded proteins from Yersinia enterocolitica. The data indicate that the O-polysaccharides as strong antigens are physiologically exposed to the immune system while lipid A and enterobacterial proteins are solely immunogenic under abnormal conditions.

Adult↗
PubMed1990

[Enteropathogenic yersinias: pathogenicity factors and new diagnostic methods].

A limited number of serotypes of Yersinia enterocolitica and Y. pseudotuberculosis is enteropathogenic for humans. During the last decade molecular biology contributed significantly to the understanding of the pathogenicity of these enteric agents. All human pathogenic Yersiniae harbour a 70-kilobase plasmid which is essential for virulence expression. Presently, thirteen plasmid-encoded polypeptides have been identified. Two of them have been identified as true outer membrane proteins and at least ten are secreted into the culture medium. Plasmid-mediated pathogenic functions are survival in serum, resistance to phagocytosis, cell adhesion, and cytotoxicity. As chromosomal determinants two invasions, one heat-stable enterotoxin and one iron-utilization system have been identified. The contribution of the iron-uptake system to mouse lethality has been clearly demonstrated. The plasmid-encoded proteins have been turned out to be more suitable antigens for serologic diagnosis of yersiniosis (immunoblotting and indirect immunofluorescence) than whole bacterial antigens.

Animals↗
PubMed1990

[Serologic diagnosis and follow-up in patients with uveitis. Antibodies to virulence antigens of Yersinia enterocolitica].

Sera from 72 patients with uveitis and sera from 93 healthy blood donors were analyzed by an immunoblot technique for antibodies to plasmid-encoded virulence associated antigens of Yersinia enterocolitica. In the group of patients with acute anterior uveitis (n = 16), antibodies of the classes IgA, IgG, IgM were significantly increased in comparison to the healthy blood donors. The presence of IgA antibodies is a sign of acute or persistent Yersinia infection. For the other forms of uveitis these antibodies were not identifiable in such a significant number of patients. After 2 years, clinical and serological investigations were carried out again in these patients. At the time of the second investigation, 25/72 (34.7%) of these patients showed intraocular inflammatory activity (group 1), but in 47/72 (65.3%) ophthalmological inflammation was no longer present (group 2). The serological investigation of group 1 and group 2 showed no significant difference in the antibody response to Y. enterocolitica. From these results we conclude that a persistent or acute Yersinia infection is a possible trigger for acute anterior uveitis. To investigate an infection with Yersinia enterocolitica, a method demonstrating antibodies to the plasmid encoded antigens of Y. enterocolitica must be employed, because the virulence and the persistence of infection can only be analyzed by this technique.

Adult↗
PubMed1989

Mechanisms involved in the pathogenesis of Yersinia infections.

Yersinia enterocolitica and Yersinia pseudotuberculosis are food-borne enterobacterial pathogens which may initiate rheumatoid diseases. By molecular genetic analysis of the pathogenicity of these species virulence gene loci could be identified on the chromosome and on a plasmid. Plasmid-encoded proteins mediate cell adherence, phagocytosis resistance, survival in serum, cytotoxicity, and collagen binding. Y. enterocolitica of serotype 0:8 is mouse-lethal and arthritogenic for Lewis rats. Mouse lethality is closely associated with the expression of a chromosome-encoded high-affinity iron transport system which enables the pathogen to acquire iron for growth in iron-deficient environments. The antibody response to virulence-associated antigens of arthritis-susceptible Lewis rats differed from that of arthritis-resistant Fisher rats: Lewis rats respond strongly to the collagen-binding protein Yop1 and weakly to the iron-transport receptor protein FyuA, whereas the reverse is found with Fisher rats. This specific antibody response of Lewis rats is suggested to be important for induction of arthritis.

Animals↗
PubMed1989

Binding to collagen by Yersinia enterocolitica and Yersinia pseudotuberculosis: evidence for yopA-mediated and chromosomally encoded mechanisms.

Binding of Yersinia enterocolitica and Yersinia pseudotuberculosis strains to type I, II, and IV collagens has been studied. Wild-type strains which harbored the 40- to 50-megadalton virulence plasmid specifically bound all three types of collagen. Curing of the virulence plasmid or Tn5 insertion in the yopA gene encoding the temperature-inducible outer membrane protein YOP1 abolished the binding of all three collagen types to Y. enterocolitica and type I and II collagens to Y. pseudotuberculosis. Full binding capacity was restored by introduction of the yopA gene into nonbinding Yersinia strains. Binding of type I, II, and IV collagens was expressed in Escherichia coli constructs harboring the yopA gene of either Y. enterocolitica or Y. pseudotuberculosis. The interaction of bacterial cells with type I collagen could be blocked by nonradiolabeled native collagens or denatured collagen but not with other serum and connective-tissue proteins. Unlabeled collagen could not displace bound radiolabeled collagen. The binding was inhibited by YOP1-specific polyclonal antibodies, in contrast to normal rabbit serum. The interaction was rapid and was quite resistant to heat treatment, to proteolytic enzymes, to various pHs in both acidic and alkaline ranges, and to the chaotropic agent urea. We propose that this newly identified interaction may be involved both in the first steps of the pathogenesis and in the complications of Yersinia infections affecting connective tissue.

Bacterial Outer Membrane Proteins↗
PubMed1989

Avidity of antibodies against released proteins of Yersinia spp: comparison of patients with or without reactive arthritis.

The avidity of IgM, IgG, and IgA class antibodies against virulence plasmid encoded proteins of yersinia, so called released proteins (RPs), was studied in the serum samples of 22 patients with yersinia triggered reactive arthritis and 22 with uncomplicated yersiniosis. The avidity of anti-RP antibodies did not differ significantly between the patient groups, even though the total amount of IgA class anti-RP antibodies was significantly higher in patients with arthritis than in those with uncomplicated yersiniosis at the early stage of infection. Earlier results with whole bacterial extracts or lipopolysaccharide as the antigens have shown an increased avidity of IgA class anti-yersinia antibodies in patients with yersinia triggered reactive arthritis. This phenomenon was not observed in antibody response against RPs, and thus production of these proteins seems unimportant at later stages of infection for the yersinia organisms stimulating the persisting and maturing antibody response in the yersinia triggered reactive arthritis.

Adult↗
PubMed1989

Immunoblot analysis of IgM, IgG, and IgA responses to plasmid encoded released proteins of Yersinia enterocolitica in patients with or without yersinia triggered reactive arthritis.

The IgM, IgG, and IgA antibody responses of patients with Yersinia enterocolitica O:3 infection were studied by immunoblotting with plasmid encoded released proteins of Y enterocolitica as the antigens. The results indicate that antibodies of all three classes are most consistently directed against the proteins of molecular weights 25,000 and 36,000. Less than two months after the onset of infection 18 of the 19 patients with yersinia triggered reactive arthritis had IgA class antibodies against the released protein of mol. wt 36,000, whereas only eight of the 17 patients with non-arthritic yersiniosis had these antibodies. The same difference between the arthritic and non-arthritic patients was observed also 8-12 months after the onset of infection.

Antibodies, Bacterial↗
PubMed1988

The microscopic double immunofluorescence technique, a method for quantitative differentiation between extra- and intracellularly located bacteria in isolated polymorphonuclear granulocytes.

A simple microscopic double immunofluorescence staining technique for the study of phagocytosis of living bacteria by human polymorphonuclear granulocytes (PMN) is presented. This technique enables the differentiation between cell-attached and ingested bacteria and allows the kinetics of phagocytosis to be monitored. The practicability and accuracy of this method is demonstrated by using two genetically defined Yersinia enterocolitica strains of different virulence, and isolated PMN resuspended in serum-free and serum-containing medium, respectively. The advantages of this method over other techniques are discussed.

Fluorescent Antibody Technique↗
PubMed1988

Analysis of the class-specific immune response to Yersinia enterocolitica virulence-associated antigens in oro-gastrically infected rabbits.

The antibody response was analysed in rabbits oro-gastrically infected (i) with virulent-(plasmid-carrying) Yersinia enterocolitica 0:3 (v-rabbits) and (ii) with the avirulent (plasmid-cured) derivative (av-rabbits). In an immunoblot assay with whole cell lysate proteins from the infecting virulent Yersinia strain, a significant IgG response was evident in convalescent-sera of v-rabbits and of av-rabbits, demonstrating that all rabbits seroconverted. However, v-rabbits mounted a stronger immune response to the cell lysate proteins than av-rabbits and the immune response persisted for a longer time. The post-challenge sera also reacted with whole cell lysate proteins of Escherichia coli and Salmonella typhimurium, indicating cross-reactivity between the different members of Enterobacteriaceae. In contrast, the antibody response against plasmid-encoded released proteins (RPs) appeared specific for infection with virulent strains in that the sera of av-rabbits failed to recognize the plasmid-encoded proteins. Six days following challenge with the virulent Yersinia strain all animals mounted a serum IgM and IgA response to RPs, followed by IgG antibodies on day 9. While the IgM and IgA serum antibody response rapidly decreased (within five-seven and eight-ten months, respectively), IgG antibodies to RPs were still present one year after challenge. Fourteen months after the first infection both the av-rabbits and the v-rabbits were reinfected with the virulent Yersinia strain and the antibody response to RPs was monitored. The v-rabbits only responded with a significant increase of IgG antibodies, indicating that they were primed to the RPs whereas the av-rabbits produced IgM, IgA and IgG specific antibodies like those seen in the primary response of v-rabbits. This study indicates that the rabbit model is helpful and adequate to analyse the character and kinetics of the antibody response during Yersinia infection.

Agglutination Tests↗
PubMed1988

Purified verotoxins of Escherichia coli O157:H7 decrease prostacyclin synthesis by endothelial cells.

Two immunologically distinct verotoxins purified from Escherichia coli C600, lysogenized with distinct temperate phages from E. coli strain 933 of serotype O157:H7, were compared by SDS-PAGE and different biological assays. The two toxins termed verotoxin 1 (VT1) and verotoxin 2 (VT2) differing in molecular weight exhibited similar biological activities. Both preparations were toxic for HeLa cells and lethal for mice. Epidemiological evidence of verotoxinogenesis in some cases of hemolytic-uremic syndrome (HUS) and the recent observations of inadequate prostacyclin production by endothelial cells associated with HUS prompted us to study the effect of purified verotoxins on prostacyclin synthesis in rat aortic tissue. Our results demonstrate a significant reduction of prostacyclin by both toxins at picomolar levels. The suppression of prostacyclin release by a lower concentration of VT2 as compared with VT1 reflects the relative potencies of these toxins in HeLa cell toxicity and mouse lethality. The results suggest an effect of verotoxins on endothelial cells and support the concept of these toxins as virulence factors in E. coli.

Animals↗