The absence of antibodies to type II collagen in established adjuvant arthritis in rats

Abstract

Utilizing an adjuvant arthritis model in rats, we examined humoral immunity to collagen and inflammation in animals with active disease and during drug therapy. Humoral immunity to types I or II collagen was not detected in the sera of rats with advanced adjuvant arthritis; this was in marked contrast to rats with type II collagen-induced arthritis which possessed serum antibodies to native and denatured type II collagen. Hind paw edema and bone pathology were monitored as parameters of inflammation. A new investigational drug, Wy-41,770, was most effective in reducing all of these aspects of inflammatory disease while indomethacin, methylprednisolone, and D-penicillamine caused a less significant diminution of only some of these parameters of inflammation. Antibodies to collagen were not detected in the sera of rats treated with the drugs under study. These data demonstrate that adjuvant arthritis can occur in rats in the absence of antibodies to types I or II collagen.

Effect of gold salts,d-penicillamine and benoxaprofen on type II collagen-induced arthritis in rats

“…Collection of blood from the retroorbital plexus was made on day 21 in order to measure type II collagen antibody titers using ELISA and serum copper and gold levels using atomic absorption. The methodology used for measurement of type II collagen antibody titers has been described in detail elsewhere [17]. Briefly, sera from rats was diluted 1:500 with Dulbecco's phosphate-buffered saline (pH 7.5) containing 0.05% Tween 80, and was incubated with native type II collagen.…”

The antiinflammatory profile of (5H-dibenzo[A, D]-cyclohepten-5-ylidene)acetic acid (WY-41,770), an agent possessing weak prostaglandin synthetase inhibitory activity that is devoid of gastric side effects

“…Wy-41,770, also inhibits the pathologic bony changes that occur in established adjuvant arthritis [17]. Joint destruction is known to involve the release of neutral proteases and acid hydrolases from lysosomes located in phagocytic cells.…”