Experimental induction of arthritis in LEW rats and antibody response to four Mycoplasma arthritidis strains.
Four Mycoplasma arthritidis strains were examined for differences in virulence for LEW rats and elicitation of antibody responses in the immunoglobulin (Ig) M and G classes and in the four IgG subclasses. Two strains were highly arthritogenic and two were relatively avirulent. When the latter strains did induce arthritis, it was significantly less severe (P less than 0.05) and developed significantly later (P less than 0.001) than in rats injected with the two virulent strains, suggesting that the low-virulence organisms are able to persist asymptomatically in rats for several weeks. None of the M. arthritidis-injected rats developed metabolism-inhibiting (MI) antibodies at any time during the 6-week observation period. Responses to other M. arthritidis antigens from all four strains were measured by enzyme immunoassay (ELISA); they were similar qualitatively but differed quantitatively. Rats injected with the two avirulent strains showed significantly lower titers of IgM antibodies (P less than 0.01) throughout the 6-week observation period and significantly lower early titers of IgG antibodies (P less than 0.05) than rats injected with the two virulent strains. In addition, peak IgM antibody titers, IgM titers measured 1 and 6 weeks after injection and IgG antibody titers measured 1 week after injection all correlated significantly with peak arthritis scores (P less than 0.05). The IgG antibody response against all four strains appeared mostly in the IgG2a and IgG2b fractions, with very little in the IgG1 and IgG2c fractions. Using immunoblotting, the immunodominant antigens of the two virulent strains appeared very similar, but the avirulent strains differed slightly from each other and from the other two. This study indicates that immune responses of rats to virulent and avirulent strains are similar but not identical and that immunogenicity for LEW rats may be a strain-specific characteristic for M. arthritidis.
Washburn
L R
LR
University of Utah School of Medicine, Department of Internal Medicine, Salt Lake City 84132.
Ramsay
J R
JR
D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis*; D001168:Arthritis / Q000276:immunology / Q000382:microbiology / Q000662:veterinary*; D001798:Blood Proteins / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D015151:Immunoblotting; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000276:immunology; D009174:Mycoplasma / Q000276:immunology* / Q000302:isolation & purification / Q000472:pathogenicity; D051381:Rats; D011917:Rats, Inbred Lew / Q000382:microbiology*; D011919:Rats, Inbred Strains / Q000382:microbiology*; D014774:Virulence
D000907:Antibodies, Bacterial; D001798:Blood Proteins; D007074:Immunoglobulin G; D007075:Immunoglobulin M