Abstract
Yersinia enterocolitica O:3 is mentioned among the most common arthritogenic pathogens. Bacterial components (including lipopolysaccharide (LPS)) may persist in the joint after eradication of infection. Having an adjuvant activity, LPS may enhance production of anticollagen antibodies, involved in the pathogenesis of rheumatoid arthritis. Furthermore, its ability to activate complement contributes to the inflammation. The aim of this work was to investigate whether Yersinia LPS (coinjected with collagen) is associated with arthritis progression or other pathological effects and to elucidate the mechanism of this association. It was demonstrated that murine mannose-binding lectin C (MBL-C) recognizes the inner core heptoses of the Rd1 chemotype LPS of Yersinia. In addition, the Rd1 LPS activates the MBL-associated serine protease 1 (MASP-1) stronger than the S and Ra chemotype LPS and comparable to Klebsiella pneumoniae O:3 LPS. However, in contrast to the latter, Yersinia Rd1 LPS was associated neither with the adjuvancity nor with the enhancement of pathological changes in animal paws/impairment of motility. On the other hand, it seemed to be more hepatotoxic when compared with the other tested endotoxins, while the enlargement of inguinal lymph nodes and drop in hepatic MBL-C expression (at the mRNA level) were independent of LPS chemotype. Our data did not suggest no greater impact Y. enterocolitica O:3 on the development or severity of arthropathy related to anticollagen antibody-induced arthritis in mice, although its interaction with MBL-C and subsequent complement activation may contribute to some adverse effects.
Highlights
Reactive arthritis (ReA), is a self-limiting disease; even 60% of patients may develop chronic arthritis [1]
To assess the possible contribution of Yersinia LPS to collagen-induced arthritis, BALB/c mice were immunized with type II chicken collagen (CII) mixed either with Yersinia wild-type LPS (6471/76-c), LPS with complete outer core (YeO3-c-R1, Ra-chemotype), or LPS reduced to the lipid A-inner core (YeO3-c-R1-M181, Rd1 chemotype), according to Takahashi et al [17]
Mice immunized with collagen type II (CII) mixed with K. pneumoniae O:3 LPS were used as a positive control
Summary
Reactive arthritis (ReA), is a self-limiting disease; even 60% of patients may develop chronic arthritis [1]. The development of ReA is considered to be associated with past genitourinary or gastrointestinal infections [2]. Yersinia enterocolitica O:3 (YeO3) is mentioned among the most common arthritogenic agents [3]. Bacteria may gain access to the circulation and be transferred to the joint either via plasma or within lymphatic cells [4]. The presence of Yersinia antigens (including LPS) was demonstrated in synovial fluid cells [5]. A strong arthritogenic potential of Y. enterocolitica O:8 LPS was demonstrated by Di Genaro et al [6] in a hamster model. Granfors et al [7] detected Yersinia LPS in leukocytes of patients with Y. enterocolitica O:3-triggered ReA even four years after infection. Wuorela et al [8] showed that in the result of intracellular processing, the majority of LPS molecules presented on the surface of monocytes are devoid of the O-polysaccharide region
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