Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalance to the Etiology of Rheumatoid Arthritis

<table class="figure-group"><tr class="fig-image" id="a"><td><object data="https://static.hindawi.com/articles/ad/volume-2015/636207/figures/636207.fig.004a.svgz" name="636207.fig.004a" type="image/svg+xml"></object></td></tr><tr class="fig-caption"><td><b>(a) </b>Serum IL-6 levels</td></tr><tr class="fig-image" id="b"><td><object data="https://static.hindawi.com/articles/ad/volume-2015/636207/figures/636207.fig.004b.svgz" name="636207.fig.004b" type="image/svg+xml"></object></td></tr><tr class="fig-caption"><td><b>(b) </b>Arthritis score</td></tr></table>

<div>Synergistic effect of bacterial toxins and autoantibodies to type II collagen in induction of arthritis in mice. Oral administration of LPS in mice receiving a subarthritogenic dose of monoclonal antibody cocktail displayed an immediate increase in serum IL-6 levels and induced arthritis within 24–48 hours, reaching a maximum score on days 7-8. Co-oral administration of LPS-adsorbent prevents the increase of serum IL-6 and development of arthritis in a dose-dependent manner.<i> Note</i>. Serum IL-6 level was increased only in old mice more than 8 months but was not observed in young mice.</div>

Autoimmune Diseases

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Figure 4: Slipping through the Cracks: Linking Low Immune Function and Intestinal Bacterial Imbalance to the Etiology of Rheumatoid Arthritis 