Immunological Responses of the Rat toMycoplasma arthritidis

Abstract

Arthritis was produced in rats by the intravenous injection of Mycoplasma arthritidis. Metabolic inhibiting antibody and indirect hemagglutinating antibody could not be detected in the sera of arthritic or convalescent animals. Nonmurine species of mycoplasma were capable of inducing metabolic inhibiting antibody in the rat. A hypothesis based upon the possible occurrence of heterogenetic antigens common to M. arthritidis and rat tissue was brought forward to explain these findings. Complement-fixing antibody to M. arthritidis was detected 3 to 4 days after injection and subsequently rose to high levels, depending upon the severity of arthritis and number of organisms injected. Animals that had recovered from intravenous or subcutaneous inoculation with M. arthritidis were resistant to subsequent infections by the organism. Immunity could be passively transferred by the intravenous injection of convalescent serum. Adsorption of the convalescent serum with antigen greatly reduced the complement fixation titer but did not significantly alter the protective properties of the serum. The presence of complement-fixing antibody could not be related to the development of immunity. An avirulent strain of M. arthritidis and a strain previously classified as M. hominis type 2 were capable of inducing resistance to subsequent injection by virulent M. arthritidis. Histological studies of rat arthritis induced by Mycoplasma arthritidis have been well described in the literature (8, 15, 16, 21), but little detailed work has been reported on antibody response or the mechanisms involved in the development of immunity. Early studies by Collier (5) and Woglom and Warren (22) indicated that the subcutaneous (sc) or intravenous (iv) injection of rats with M. arthritidis resulted in the development of resistance to reinfection. Both of these studies failed MATERIALS AND METHODS Strains used. The sources of the mycoplasmas used in this study are listed in Table 1. The pathogenicity for rats of strains previously called M. hominis type 2, Campo, was established previously (4). To increase virulence, M. arthritidis strains 158 and 14124 were passaged in rats 10 times by sc injection. Mycoplasmas cultured from the resulting abscesses were injected sc into normal rats. The passaged strains were designated 158 PlO and 14124 PIO, respectively. The virulence of these organisms was similar to that of freshly isolated strains (B. C. Dole and L. Rowland, unpublished data). Unless otherwise stated, all experiments reported in this study were conducted with M. arthritidis strain 158 P10. Media. The medium used for maintenance of mycoplasma strains consisted of mycoplasma agar 930

Chronic arthritis of rabbits induced by mycoplasmas II.antibody response and the deposition of immune complexes

“…It has been suggested that in certain other mycoplasma-induced arthritides, chronicity is dependent upon retention of organisms (25). In murine arthritis the persistence of mycoplasmas may be due to the inability of these animals to produce sufficient neutralizing, or MI, antibodies to clear the organisms from joint tissues (26)(27)(28)(29). In the rabbit disease described in this report, however, other mechanisms of chronic inflammation must be sought to explain the continuation of disease activity.…”

“…Three rabbits from the M arthritidis-injected group, 3 from the M pulmonis-injected group, 1 from the broth-injected group, and 1 normal control animal were killed at intervals of 1,2,4,7,12,20,31, and 52 weeks postinoculation. In addition, 8 rabbits each from the mycoplasma-injected groups and 7 from the broth-injected group were set aside for observation throughout the entire year and were bled for immunologic studies at intervals of 1,3, and 5 days and 1,2,3,4,7,12, 16,20,26,31,42, and 52 weeks postinoculation. Tissues were removed at autopsy for microbiologic, histologic, and immunologic examination as described previously (1).…”

Effect of Animal Passage on Arthritogenic and Biological Properties of Mycoplasma arthritidis

“…Rat arthritis induced by Mycoplasma arthritidis has been studied extensively in relation to clinical and histological characteristics (10,24,27,34). The immunological responses of the host have been described (5,15,17), and it has recently been suggested that a heterogenetic antigen common to M. arthritidis and rat tissue may play a role in the pathogenesis of this disease (5). In spite of these studies, many questions remain unanswered, such as the mechanism of immunity to reinfection and the pathogenesis of the spontaneous and experimental disease.…”

Studies on the infectious etiology of rheumatoid arthritis

“…Williams particularly interesting in view of the fact that this species produces arthritis in rats. M arthritidis also produces a chronic proliferative arthritis of mice with periods of exacerbation and remission, and the histopathology of this disease closely resembles that of human RA (31,32).…”

“…T h e presence or absence of circulating antibodies has been used as evidence for or against a It should be pointed out that failure to detect antibodies against a particular species does not necessarily indicate the absence of that organism, since we have shown that MI antibodies cannot be detected in rats experimentally infected with M arthrztidis (31).…”