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A Toivanen

Publications and source records attributed to A Toivanen.

At least 91 records · Page 5Linked to original sources
PubMed1989

Yersinia antigens in synovial-fluid cells from patients with reactive arthritis.

We examined synovial-fluid cells from 15 patients with reactive arthritis after yersinia infection for the presence of yersinia antigens. Extensive bacterial cultures of the synovial fluid were negative. All the samples were studied by immunofluorescence with use of a rabbit antiserum to Yersinia enterocolitica O:3 and a monoclonal antibody to Y. enterocolitica O:3 lipopolysaccharide. Synovial-fluid cells from 41 patients with other rheumatic diseases served as controls. Synovial-fluid cells from 10 patients with reactive arthritis after yersinia infection stained positively on immunofluorescence; rabbit antiserum and the monoclonal antibody yielded similar results. In most patients the percentage of positive cells ranged from 1 to 10 percent, but in one patient nearly all the cells in the sample stained strongly. Most of the positively stained cells were polymorphonuclear leukocytes, but yersinia antigens were also found in mononuclear phagocytes. All the control samples were negative. Synovial-fluid cell deposits from nine patients were also studied by Western blotting with use of the same antibodies. The results were positive in six of the nine cell deposits from patients with reactive arthritis and in none of the 10 cell deposits from control patients with rheumatoid arthritis. We conclude that in patients with reactive arthritis after yersinia infection, microbial antigens can be found in synovial-fluid cells from the affected joints.

Adult↗
PubMed1989

Combined interferon and vinblastine treatment of advanced melanoma: evaluation of the treatment results and the effects of the treatment on immunological functions.

Thirteen patients with metastatic malignant melanoma received interferon alpha-2a (Roferon-A) and vinblastine. The interferon dosage was increased from 3 x 10(6) IU to 9 x 10(6) IU daily in 10 weeks and thereafter 9 x 10(6) IU was administered three times weekly intramuscularly. Vinblastine (0.075-0.15 mg/kg) was given every third week intravenously. One of the ten evaluable patients had partial remission (PR) (11%) for 10 months. The diseases was stabilized (NC) in three patients (30%) for 3, 6 and 9 months. Progression (PD) occurred in six patients. The treatment time varied from 5 weeks to 44 weeks. The median survival time from the beginning of this combination treatment was 5 months. The most common side-effects were fever, fatigue, loss of taste, weight loss and neutropenia. The mitogen response to phytohemagglutinin and purified protein derivative of tuberculin decreased in all patients. The response to concanavalin A decreased less and began to increase again in the patients with PR and NC. The natural killer cell activity in PD patients decreased more than in the patients with PR and NC. The ratio of T4/T8-positive cells was restored in PR + NC patients but rose in PD patients indicating a difference in the immunomodulatory effect of the combination or of the advanced disease itself on T-cell function in PD patients. This combination of daily interferon and vinblastine did not prove to be effective in melanoma. The depression of immunological functions, which was more marked in patients with PD, might indicate that vinblastine in this combination counteracts the immunostimulatory effect of interferon.

Adult↗
PubMed1989

Immunological and bacteriological aspects of reactive arthritis.

It is apparent that in the development of reactive arthritis the patient fails in his first line of defence against the invading microorganism. This results in persistence of the microorganism probably in or close to the intestinal epithelium. Microbial antigens may appear also in the circulation, perhaps as part of the immune complexes, or within cellular elements. Through these transportation mechanisms they enter the synovium, triggering an inflammatory process that leads to reactive arthritis.

Antibodies, Bacterial↗
PubMed1989

Clinical manifestations of Yersinia pseudotuberculosis infection in children.

The clinical manifestations of infection were analysed during an outbreak of 34 cases of Yersinia pseudotuberculosis serotype Ia infection. The diagnosis was based on the results of enzyme immunoassay and verified by stool culture in five cases. The first four patients were pupils from the same school, and information on any signs and symptoms of infection was obtained by questionnaire from pupils of the school. A blood sample was obtained from 101 children. Strong IgM and IgG antibody responses to Yersinia pseudotuberculosis Ia were found in 13 (25%) of the 52 pupils who reported signs and symptoms of infection and in 9 (18%) of the 49 with no manifestations of infection. The vigorous immune response also resulted in effective opsonization of the causative microorganism. The most common symptoms were fever and abdominal pain. Three children operated on because of suspected appendicitis were found to have mesenteric lymphadenitis. Only one patient developed reactive arthritis. Analysis showed that a remarkable proportion of Yersinia pseudotuberculosis infections may be subclinical, and that individual Yersinia pseudotuberculosis strains may have different capacities to cause postinfection complications.

Adolescent↗
PubMed1989

Comparison of bacteria with and without plasmid-encoded proteins as antigens for measurement of immunoglobulin M, G, and A antibodies to Yersinia enterocolitica by enzyme-linked immunosorbent assay.

Yersinia enterocolitica serovar O:3 bacteria with and without plasmid-encoded proteins were compared as antigens in an enzyme-linked immunosorbent assay. Good correlations between the two antigen preparations were obtained for immunoglobulin M (IgM), IgG, and IgA antibodies of patients with yersiniosis. For routine diagnostic purposes, these antigens are considered equal.

Adult↗
PubMed1989

Inhibition of polymorphonuclear leucocyte functions in vivo by Yersinia enterocolitica lipopolysaccharide.

A single intravenous injection of 5 micrograms of Yersinia enterocolitica lipopolysaccharide (LPS) inhibits rabbit polymorphonuclear leucocyte (PMN) chemotaxis, enzyme secretion, and respiratory burst activation in response to partially purified rabbit C5a and leucotriene B4 (LTB4). Respiratory burst activation is also inhibited in response to platelet activating factor (PAF). In contrast, all these responses to n-formyl-methionyl-leucyl-phenylalanine (FMLP) remain unaltered. This LPS does not modulate PMN activation in vitro or activate the respiratory burst. Thus Y enterocolitica LPS acts in vivo by inhibiting PMN responses to endogenous mediators of inflammation. This inhibition presumably impairs the elimination of pathogens and might, therefore, provide favourable conditions for induction by bacteria of further immunological consequences.

Animals↗
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↗
PubMed1989

[Reactive arthritis].

Reactive arthritis is an abacterial form of arthritis that develops after infection at a site distant from the affected joint(s). The condition has long been recognised, often under the name of Reiter's syndrome. During recent years a number of research teams have published new findings concerning the pathogenesis of reactive arthritis which may also prove to be of importance for other rheumatic diseases. The clinical picture, treatment and prognosis of reactive arthritis are also discussed in the article.

Arthritis, Reactive↗
PubMed1989

Serum opsonic capacity against Yersinia enterocolitica O:3 in yersiniosis patients with or without reactive arthritis.

The opsonic capacity of 45 sera from patients with reactive arthritis after Yersinia enterocolitica O:3 infection and of 45 matched sera from yersiniosis patients without post-infection complications was studied at 1-3 months, 5-8 months and 12-20 months after the onset of the infection. Antibody-mediated opsonization of virulence-plasmid-containing Y. enterocolitica O:3 was studied by measuring complement-fixation on opsonized bacteria and opsonophagocytic function of the polymorphonuclear leucocytes (PMN). The PMN response against bacteria pre-opsonized by heat-inactivated sera was measured by using a chemiluminescence (CL) assay. The fixation of complement Clq and C3 on bacteria was determined by flow cytometry using fluorescein-conjugated Clq- and C3c-antisera. All the sera were strongly opsonic at the onset of the infection, and this capacity persisted in most of the patients still at the end of the follow-up. No difference was observed in complement-fixing capacity between the sera of the two groups, but the sera from arthritic patients showed stronger augmentation of PMN CL response at the early phase of the infection (P = 0.005 in the presence of complement, P = 0.04 in the absence of complement). These results suggest that enhanced opsonic capacity may play a role in the development of Yersinia-triggered reactive arthritis by leading to strong activation of the PMN and, consequently, to release of inflammatory mediators.

Antibodies, Bacterial↗
PubMed1989

Synovial T lymphocyte recognition of organisms that trigger reactive arthritis.

Reactive arthritis (ReA) is believed to be "triggered' by infection with certain bacteria. When the proliferative responses of mononuclear cells (MC) obtained from the synovial fluid (SF) of ReA patients were examined, it was found that they responded maximally to the specific organism responsible for the preceding infection. The response was shown to be due to Class II MHC-restricted T cells by inhibition experiments using cyclosporin A and monoclonal antibodies. Significant SFMC responses to additional organisms associated with ReA were also recorded; since there was no serological evidence of preceding infection by these organisms, this finding suggests that these bacteria share common T cell-recognized antigenic epitopes. The corresponding responses by peripheral blood mononuclear cells (PBMC) were much lower and often barely detectable, whereas their responses to PHA were consistently higher than those of SFMC. These results, combined with evidence that bacterial antigens localize in the joint, indicate that a bacteria-specific, T-cell-mediated response may play a central role in the pathogenesis of ReA.

Antigens, Bacterial↗
PubMed1988

Arthritis-associated changes in flow cytometric characteristics of cultured synovial fibroblasts.

Synovial fibroblasts cultured from patients with rheumatoid or reactive arthritis and from controls were studied by flow cytometry, spectroscopy, and electron microscopy. Analysis of 29 cell lines revealed consistent differences between arthritic and normal fibroblasts. Cells cultured from inflamed synovial tissue exhibited higher autofluorescence than did control fibroblasts, and displayed exceptional light scatter properties in flow cytometry, indicating changes in cytoplasmic structures. Electron microscopic examination of the fibroblasts from arthritic synovial tissue revealed large numbers of round, swollen, laminated, mitochondrion-like bodies, which were not observed in the control fibroblasts. The changes observed by flow cytometry (light scatter and autofluorescence) coincided with the presence of the mitochondrion-like organelles. The strong autofluorescence observed in the arthritic fibroblasts resembled the fluorescence spectrum of mitochondrial flavoproteins. These data suggest that persistent metabolic and structural changes have occurred in the mitochondria of synovial fibroblasts and inflammatory synovial tissue. The usefulness of flow cytometry in identifying such cells is described.

Arthritis↗
PubMed1988

Luminol-enhanced chemiluminescence of peripheral blood leukocytes as an early indicator of graft take after allogeneic bone marrow transplantation in patients with acute myelogenous leukaemia.

The luminol-enhanced chemiluminescence (CL) of peripheral blood leukocytes was studied daily in five patients with acute myelogenous leukaemia (AML) in first remission, who were undergoing allogeneic bone marrow transplantation (BMT). The CL was measured after stimulation of leukocytes with opsonized zymosan in highly diluted whole blood. All patients had an undetectable CL level on day +7, post BMT, simultaneously with severe pancytopenia caused by the pre-conditioning for BMT. Subsequently, CL started to rise, reaching the maximum level, twice that of healthy controls, on day +11. This preceded the rise of blood leukocytes above 1.0 x 10(9) l.-1 and that of neutrophils above 0.5 x 10(9) l.-1 by 3-14 days, but coincided with the appearance of large unstained cells (LUC; a parameter given by a Technicon H 6000 blood analyzer). One of the patients later had a transient decline of CL. This preceded the fall in white blood count and platelets by 7 days, suggesting marrow suppression. We conclude that in AML the measurement of leukocyte CL is a more sensitive test for prediction of graft take than the conventional blood counts.

Blood Cell Count↗
PubMed1988

Serum IgA deficiency and anti-IgA antibodies in pernicious anemia.

Three pernicious anemia (PA) patients with selective IgA deficiency and anti-IgA antibodies in their sera were followed for over 3 years. After instituting therapy with cyanocobalamin there was a slight increase in the anti-IgA antibodies. After 1 year the titers of anti-IgA antibodies in the sera of these patients declined significantly as compared to the values before treatment (P less than 0.02), and after 2 years one patient had no measurable anti-IgA antibodies, yet no IgA appeared in the serum of any of the three. Further, in a medium with no anti-IgA the lymphocytes of these patients were not capable of producing IgA in vitro. Thus, the reason for the IgA deficiency in PA appears to be linked to the function of B cells rather than to anti-IgA antibodies.

Adolescent↗