Abstract:Eight-week old conventional female Swiss mice were inoculated intravenously with Yersinia enterocolitica O:3. A second group of normal mice was used as control. Five mice from each group were bled by heart puncture and their spleens were removed for spleen cell collection on the 3rd, 5th, 7th, 10th, 14th and 21st day after infection. Immunoglobulin-secreting spleen cells were detected by the isotypespecific protein A plaque assay. Total immunoglobulin levels were determined in mouse serum by single radial immu… Show more
“…The production of autoantibodies may result from polyclonal B lymphocyte activation. We have shown that this association does occur in mice infected with Y. enterocolitica O:3 (22).…”
Section: Discussionmentioning
confidence: 69%
“…We have previously demonstrated that conventional Swiss mice infected with the same strain of Y. entero- colitica developed polyclonal activation of B lymphocytes. This activation was not limited to certain isotypes of immunoglobulins since the number of secretory cells of all isotypes was increased, but IgG 2a -secreting cells did increase more strongly, compared to controls (23).…”
Section: Discussionmentioning
confidence: 84%
“…Regarding the pathogenesis of reactive arthritis, one hypothesis is that the autoimmune response seen in some patients with yersiniosis is the result of the polyclonal activation of B lymphocytes and concomitant autoantibody development. In fact, polyclonal activation of B lymphocytes in conventional Swiss mice infected by Y. enterocolitica O:3 strain was first demonstrated in our laboratory (23). On the one hand, it has been postulated that LPS may be one factor responsible for reactive arthritis (8); on the other, the role of Yersinia outer membrane proteins (Yops) in the pathogenesis of reactive arthritis has not been fully elucidated yet (21).…”
The potential sequelae of intestinal infection with Yersinia enterocolitica include reactive arthritis, erythema nodosum, Reiter's syndrome and other autoimmune diseases. The role of the immune response in the pathogenesis of these diseases has not been fully defined, but autoimmune manifestations may be a consequence of the increase in autoantibodies as a result of polyclonal B-cell activation induced by Yersinia. We investigated the effects of Y. enterocolitica O:3 derivatives on B lymphocyte activation in vivo. Groups of five specific pathogen free (SPF) Swiss mice were inoculated with bacterial cell extract, Yersinia outermembrane proteins (Yops) or lipopolysaccharide (LPS) obtained from Y. enterocolitica O:3 and their immunoglobulin-secreting spleen cells were detected by isotype-specific protein A plaque assay. The presence of specific anti-Yersinia antibodies and autoantibodies was determined in mouse sera by ELISA. In all experiments a marked increase in the number of secretory cells of different isotypes was observed as early as the third day after inoculation. IgG and IgM anti-Yersinia antibodies were detected in the sera of all inoculated mice, and autoantibodies against myosin in the sera of those inoculated with bacterial cell extract. The sera from animals stimulated with LPS reacted with myelin, actin and laminin, while the sera from mice inoculated with Yops reacted with myelin, thyroglobulin and cardiolipin. These results suggest that SPF Swiss mice inoculated with any one of the Y. enterocolitica derivatives tested exhibited polyclonal activation of B lymphocytes as a result of stimulation by various bacterial components and not only LPS stimulation.
“…The production of autoantibodies may result from polyclonal B lymphocyte activation. We have shown that this association does occur in mice infected with Y. enterocolitica O:3 (22).…”
Section: Discussionmentioning
confidence: 69%
“…We have previously demonstrated that conventional Swiss mice infected with the same strain of Y. entero- colitica developed polyclonal activation of B lymphocytes. This activation was not limited to certain isotypes of immunoglobulins since the number of secretory cells of all isotypes was increased, but IgG 2a -secreting cells did increase more strongly, compared to controls (23).…”
Section: Discussionmentioning
confidence: 84%
“…Regarding the pathogenesis of reactive arthritis, one hypothesis is that the autoimmune response seen in some patients with yersiniosis is the result of the polyclonal activation of B lymphocytes and concomitant autoantibody development. In fact, polyclonal activation of B lymphocytes in conventional Swiss mice infected by Y. enterocolitica O:3 strain was first demonstrated in our laboratory (23). On the one hand, it has been postulated that LPS may be one factor responsible for reactive arthritis (8); on the other, the role of Yersinia outer membrane proteins (Yops) in the pathogenesis of reactive arthritis has not been fully elucidated yet (21).…”
The potential sequelae of intestinal infection with Yersinia enterocolitica include reactive arthritis, erythema nodosum, Reiter's syndrome and other autoimmune diseases. The role of the immune response in the pathogenesis of these diseases has not been fully defined, but autoimmune manifestations may be a consequence of the increase in autoantibodies as a result of polyclonal B-cell activation induced by Yersinia. We investigated the effects of Y. enterocolitica O:3 derivatives on B lymphocyte activation in vivo. Groups of five specific pathogen free (SPF) Swiss mice were inoculated with bacterial cell extract, Yersinia outermembrane proteins (Yops) or lipopolysaccharide (LPS) obtained from Y. enterocolitica O:3 and their immunoglobulin-secreting spleen cells were detected by isotype-specific protein A plaque assay. The presence of specific anti-Yersinia antibodies and autoantibodies was determined in mouse sera by ELISA. In all experiments a marked increase in the number of secretory cells of different isotypes was observed as early as the third day after inoculation. IgG and IgM anti-Yersinia antibodies were detected in the sera of all inoculated mice, and autoantibodies against myosin in the sera of those inoculated with bacterial cell extract. The sera from animals stimulated with LPS reacted with myelin, actin and laminin, while the sera from mice inoculated with Yops reacted with myelin, thyroglobulin and cardiolipin. These results suggest that SPF Swiss mice inoculated with any one of the Y. enterocolitica derivatives tested exhibited polyclonal activation of B lymphocytes as a result of stimulation by various bacterial components and not only LPS stimulation.
“…Polyclonal activation of B lymphocytes in Swiss mice infected with a low-pathogenicity strain, Y. enterocolitica O:3, was first demonstrated in our laboratory (29). Furthermore, Crespo et al (7) demonstrated that Y. enterocolitica O:3 derivatives, such as LPS and Yops, induce polyclonal activation of B lymphocytes.…”
Polyclonal lymphocyte stimulation is one of the immunomodulatory mechanisms induced by arthritogenic pathogens. In this study we examined the polyclonal activation potential of a virulent strain of Y. enterocolitica serotype O:8 (WA 2707+) and its plasmidless isogenic pair (WA 2707−). SPF Swiss mice were infected intragastrically and spleen cells were obtained on days 7, 14, 21, 28, 35 and 42 after infection. The number of cells secreting nonspecific immunoglobulins of IgG, IgM and IgA isotypes was determined by the ELISPOT technique. The presence of serum‐specific antibodies was investigated by ELISA and the presence of autoantibodies by dot‐blot assay. Although the patterns of infection of the two bacterial strains were almost the same, only the animals infected with the virulent strain presented clinical anomalies. Neither arthritic nor inflammatory signs were observed in the joints of the infected animals. The greatest activation observed was that of the nonspecific IgM‐secreting cells, and their peak of secretion occurred between the 28th and the 42nd day after infection, for both strains of Y. enterocolitica O:8. Only the animals infected with the virulent strain (WA 2707+) produced IgG‐specific antibodies in the serum, from the 28th day after infection. The serum of animals infected with either strain showed reactivity to all the autologous constituents tested, mainly on the 28th and 42nd day after infection. It was concluded that infection of mice with either the virulent strain of Y. enterocolitica O:8 or with its plasmidless isogenic pair resulted in the polyclonal activation of the splenic B lymphocytes including some autoreactive clones.
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