Analysis of IgA antibodies to lipopolysaccharide in Yersinia-triggered reactive arthritis.
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Antibody Specificity↗
Biomedical subjects
K Granfors
Publications and source records attributed to K Granfors.
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↗
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↗
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↗
[New data on the pathogenesis of reactive arthritis].
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Arthritis, Infectious↗
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↗
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↗
B-cells in the chicken harderian gland.
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Animals↗
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↗
Expression of B-L and Bu-1 antigens in chickens bursectomized at 60 h of incubation.
Differences in expression between B-L (chicken class II major histocompatibility complex antigen) and Bu-1 B cell antigens were found in normal animals by using monoclonal antibodies and flow cytometric immunofluorescence analysis. Fluorescence intensity profile was used in assaying cell surface density of antigen molecules. The density of B-L antigen on the cell surface is apparently low in immature and high in mature cells, whereas the density of Bu-1 antigen does not vary in cells at different maturational stages. The existence of B-L+ and Bu-1+ cells in chickens bursectomized at 60 h of embryonic development (Bx) is demonstrated, indicating that neither B-L or Bu-1 antigen is exclusively specific for cells differentiated in the bursa. The densities of B-L and Bu-1 molecules on lymphoid cells in Bx chickens are similar to those of controls. However, the number of B-L+ and Bu-1+ cells was decreased in Bx chickens. We conclude that the extrabursal site where Bx B cells mature has an ability similar to that of the bursa to induce and enhance the expression of B-L and Bu-1 antigens. However, only few B cells proliferate and/or are released into the circulation. Further, the extrabursal site unequivocally lacks the most important function of the bursa, the creation and expansion of antibody diversity.
Aging↗
Antibody-forming capacity of B cell-deficient chickens reconstituted with limiting numbers of B cell precursors.
To examine the antibody-forming capacity of neonatally cyclophosphamide-treated chickens reconstituted with limiting numbers of B cell precursors, we analyzed their antibody responses to six unrelated antigens. Our results demonstrate that about 10 x 10(6) bursal cells are needed in this adoptive cell transfer model to restore normal immune competence to B cell-deficient birds. From our earlier data we know that with low repopulating cell numbers (less than 10 x 10(6) cells) developing bursal follicles are of clonal origin. Ten million cells repopulate about 40%, i.e. about 4 x 10(3) of the bursal lymphoid follicles. Assuming the clonal origin of the follicles these results imply that the B cell system of birds receiving this dose is derived from less than 5 x 10(3) precursor cells. At the lowest reconstituting dose (1.25 x 10(6) cells) most birds do not respond to the antigens studied. However, their B cell system is derived from only about 500 precursor cells. Because the antibody repertoire of a normal chicken was estimated to be at least 10(6) our results suggest that each precursor gives rise to a large number (greater than 200) of immunoglobulin V-region gene variants during its clonal proliferation in the bursa. Our results are thus consistent with the proposed "hyperconversion" mechanism of generation of antibody diversity in the chicken and provide quantitative data useful for estimating what such somatic modification rates might be.
Animals↗
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↗
IgM, IgG, and IgA antibodies in Yersinia infection.
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Antibodies, Bacterial↗
Factors associated with the development of reactive arthritis.
The role of the causative microorganism in the generation of reactive arthritis is decisive, but host factors are also of major importance. Patients who develop reactive arthritis after Yersinia enteritis show several interesting features in the immunological defence against Yersinia when compared to those who recover uneventfully. When all these peculiarities are taken together, they strongly indicate that in the patients developing reactive arthritis the causative microorganism enters host tissues to persist within the body for prolonged periods of time.
Antibody Formation↗
Susceptibility to tolerance induction of bursal and peripheral B cells.
We investigated cellular aspects of immunological tolerance to protein antigens in chickens by examining the immune responses of bursal and splenic cells from tolerant or normal chickens after transfer into cyclophosphamide (CP)-treated recipients. Newly-hatched chicks were made tolerant to bovine serum albumin (BSA) by injection of 100 mg of the antigen. When bursa cells from 4-day-old BSA-unresponsive chicks were transferred into CP-treated recipients, the reconstituted birds were able to respond to a subsequent injection of BSA almost as well as normal birds, and as well as CP-treated birds that had been reconstituted with normal bursa cells. To investigate whether the presence of the BSA antigen might affect recovery from tolerance, we injected CP-treated recipients with BSA at the time of transfer of bursal cells. The presence of the antigen prevented the recovery of the anti-BSA response in reconstituted birds. When spleen cells from 6.5-week-old unresponsive chicks were transferred into CP-treated recipients, no recovery of responsiveness to BSA could be demonstrated. A likely reason for the failure of splenic B cells to recover responsiveness on transfer is their inability to generate somatic variants of Ig genes in the same way as bursal stem cells. Thus, when the bursa involutes, the chicken's antibody repertoire may be frozen in a less adaptable state than that of a mammal.
Animals↗
Role of antibodies in the opsonization of Yersinia spp.
We have determined the opsonic capacity of specific antibodies in patient sera obtained after Yersinia infection. The results indicate that Yersinia antibodies lead to complement activation through the classical pathway, thus overcoming the inhibition of complement-mediated opsonization in the absence of specific antibodies provided by the virulence plasmid in Yersinia enterocolitica and Yersinia pseudotuberculosis. Further, antibodies against plasmid-encoded structures, the Yersinia outer membrane proteins (YOPs), are not necessary in this effect. This is indicated by two facts. (i) Monoclonal antibodies directed against the O polysaccharide of Y. enterocolitica O:3 are capable of opsonizing the plasmid-containing bacteria through C1q binding. (ii) Rabbit antisera show opsonic activity when obtained by immunization both with plasmid-containing Y. enterocolitica expressing the YOPs and a plasmid-cured variant not expressing these proteins.
Antibodies, Bacterial↗
IgA class antibodies against Yersinia enterocolitica O:3 in patients with thyroid disease.
IgM, IgG and IgA class serum antibodies against Yersinia enterocolitica O:3 and O:9 and Yersinia pseudotuberculosis 1a and 3 in 41 patients with thyroid disease and 50 healthy control persons were measured by enzyme-linked immunosorbent assay (ELISA). Concentrations of antibody levels against Yersinia enterocolitica O:9 and Yercinia pseudotuberculosis 1a and 3 did not differ significantly between the patients and controls. The median value of IgA class antibody Yersinia enterocolitica O:3 was 7.5 relative units (EIU, percentage of the reference serum) in the patients with thyroid disease and 0.7 EIU in the controls (P less than 0.01; Mann-Whitney's U-test), whereas IgM and IgG class antibodies did not show this difference. IgA class serum antibodies were especially high in patients with autoimmune thyroid diseases. These findings and two case reports support the concept that there may be a causal relationship between infections with Yersinia enterocolitica O:3 and autoimmune thyroid diseases.
Adolescent↗
Rheumatoid factors in Yersinia-triggered reactive arthritis.
Total rheumatoid factor (RF) activity and RF isotypes were measured in the sera of 33 patients with Yersinia infection using enzyme-linked immunosorbent assay. Twenty out of 33 patients developed reactive arthritis as a postinfectious complication. Yersinia infection does not seem to stimulate formation of RFs. The serum samples were practically negative, except two consecutive samples of one patient with Yersinia enterocolitica 0:3 triggered reactive arthritis which were strongly positive for all RFs tested. Although in Yersinia triggered reactive arthritis continuous response against Yersinia is seen, especially in the form of persisting IgA response, RF do not seem to be involved.
Adolescent↗