4.1 Article

Lactobacillus rhamnosus Exopolysaccharide Ameliorates Arthritis Induced by the Systemic Injection of Collagen and Lipopolysaccharide in DBA/1 Mice

Journal

ARCHIVUM IMMUNOLOGIAE ET THERAPIAE EXPERIMENTALIS
Volume 60, Issue 3, Pages 211-220

Publisher

SPRINGER BASEL AG
DOI: 10.1007/s00005-012-0170-5

Keywords

Exopolysaccharide; Lactobacillus rhamnosus; Collagen-induced arthritis; LPS; Collagen-specific antibodies

Categories

Funding

  1. Jagiellonian University College of Medicine [K/ZDS/000678]
  2. Ministry of Science and Higher Education (Poland) [N N401 042438]

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Oral administration of some probiotic bacteria (e.g. Lactobacillus rhamnosus) attenuates various types of experimental arthritis, including collagen-induced arthritis (CIA) and inhibits arthritogenic autoantibodies. Much less is known about the possible anti-arthritogenic properties of exopolysaccharide (EPS), the major component of lactic bacteria biofilm. In this study, we asked the question whether systemic administration of EPS derived from L. rhamnosus KL37 depresses the production of anti-collagen IgG and affects the development of CIA in DBA/1 mice. Arthritis was induced employing two models of active CIA, in which mice were immunized with type II collagen (CII) either in the presence of lipopolysaccharide (LPS; mild arthritis with moderate CII-specific IgG production) or with Complete Freund's Adjuvant and LPS (severe arthritis with massive CII-specific IgG production). Passive CIA was induced by intravenous injection of CII-specific monoclonal antibodies and LPS. Disease progression, the incidence and severity of arthritis, were determined. Serum concentration of CII-specific IgG was measured by enzyme-linked immunosorbent assay. Systemic administration of EPS markedly reduced CII-specific antibody production. Moreover, EPS significantly ameliorated arthritis in the active models of CIA, especially, when LPS alone was used as an adjuvant. In contrast, when arthritogenic antibodies were injected to mice in high amounts, the effect of EPS on the development of passive CIA was negligible and transient. These results show that EPS can suppress active CIA by the inhibition of arthritogenic antibodies production. Therefore, we suggest that EPS or EPS-producing probiotics may be promising agents for the supporting therapy of patients with rheumatoid arthritis.

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