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Gold complexes are used in the treatment of rheumatoid arthritis for some 60 years by now. The authors used therefore a gold complex, sodium aurothiosulphate (ATSS) to influence the experimental model of arthritis induced by immunization with type II collagen in laboratory rats. To the first group of laboratory rats ATSS was administered concurrently with the first immunization dose, to the second group with the second immunization dose and to the third group in the course of arthritis. ATSS was administered to individual groups every week by the i. m. route, 20 mg/kg body weight. In all three groups a reduction of arthritic symptoms was observed, however, in group three to a much lesser extent than in groups one and two. The results of the experiment indicate clearly that ATSS was able to suppress the development of collagen induced arthritis, if administered not later than with the second immunization dose. As the formation of antibodies against type II collagen was not suppressed, it may be assumed that the activation of the complement system was blocked by the bond of the gold complex with the C1q component. It has been proved already previously that the interaction of C1q with gold complexes is very rapid.

For the determination of antibodies against collagen in different rheumatic diseases the authors elaborated two serological techniques. It was particularly the passive haemagglutination, which proved to be little sensitive and insufficiently reproducible. Therefore, for the determination of antibodies against collagen the authors introduced the ELISA method as one of the varieties of enzyme immunoanalysis, giving more precise results. Both methods were compared and it has become apparent that the ELISA method is more reliable and more suitable for the determination of antibodies against collagen.

Using the ELISA method, the authors assessed titres of antibodies to collagen type I, II and III in serum of patients with juvenile chronic arthritis (JCA). The results were compared with antibody titres in patients with rheumatoid arthritis (RA). Elevated antibody titres to all collagen types were found, as compared with age-matched controls. The mean titres in patients with RA were higher than in the group with JCA. Investigation of a correlation between the collagen antibody titres and values of the sedimentation rate after one hour revealed a statistical relationship only in collagen type II in patients with RA.

To laboratory rats of Wistar strain (Ipcv: Wist) native collagenous types of pig cartilage--II, IX and XI and the denatured type XI were administered. The first immunization dose, 0.5 mg collagen per experimental animal, was administered in incomplete Freund adjuvant and the second immunization dose (collagen in solution) followed after 7 days and was administered by the i.p. route. Inflammatory arthritis of the small interphalangeal, metatarsophalangeal and tarsal joints developed between the 11th and 17th day of the experiment in rats immunized with native collagen type II and XI--60% of the animals were affected. The histological findings corresponded to the course of arthritis, however, the articular destructive changes after administration of collagen type XI were more severe than after type II. The changes were evaluated by X-ray and by means of thermovision. The antibody levels against different types of collagen assessed by means of the ELISA test reached peak values between the 13th and 20th day of the experiment. In the group of rats immunized by collagen type IX and the denatured type XI arthritis did not develop. The antibody response in the group of rats immunized with type IX was similar as in the group immunized with types II and XI. Histological examination confirmed some changes in the joints of rats immunized with collagen type IX, while in the joints of rats immunized with denatured collagen type XI no changes were found.