Lipopolysaccharide accelerates collagen-induced arthritis associated with rapid and continuous production of inflammatory mediators and anti-type II collagen antibody

Tanaka, S.; Toki, T.; Akimoto, T.; Morishita, K.

Microbiology and Immunology

2013


ISSN/ISBN: 0385-5600
DOI: 10.1111/j.1348-0421.12052
Accession: 036840580

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Abstract
Collagen-induced arthritis (CIA) is an animal model for rheumatoid arthritis (RA). Lipopolysaccharide (LPS) is known to accelerate CIA, however, the pathogenetic mechanisms are not yet fully understood. In this study, we show marked elevation of mRNA expression levels of inflammatory mediators, such as tumor necrosis factor alpha (TNF?), interleukin (IL)-1? and macrophage inflammatory protein-2 (MIP-2), in the arthritic paws and anti-type II collagen (CII) antibody level in the serum before the onset of arthritis by LPS injection in CII-immunized mice. The gene expression was rapid and continuous after direct activation of nuclear factor ?B. The mRNA levels of TNF?, IL-1? and MIP-2 in addition to matrix metalloproteinases and the receptor activator of nuclear factor ?B ligand were increased with the development of arthritis and positively correlated with clinical severity, and were also associated with histopathology. Moreover, anti-TNF? neutralizing antibody inhibited the development of LPS-accelerated CIA, and single injection of recombinant mouse TNF? induced elevation of the anti-CII antibody level, suggesting TNF? may contribute to the development of arthritis by both initiation of inflammation and production of autoantibodies. These data suggest LPS may exacerbate RA associated with rapid and continuous production of inflammatory mediators and autoantibodies.

Lipopolysaccharide accelerates collagen-induced arthritis associated with rapid and continuous production of inflammatory mediators and anti-type II collagen antibody