Toxicity but not arthritogenicity of Mycoplasma arthritidis for mice associates with the haplotype expressed at the major histocompatibility complex

Cole, Barry C.; Thorpe, R N; Hassell, Lewis; Washburn, Leigh Rice; Ward, John

doi:10.1128/iai.41.3.1010-1015.1983

Cited by 29 publications

(12 citation statements)

References 14 publications

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“…The crossreaction observed between anti-M. arthritidis and M. pulmonis ELISA antigens was not reduced by addition of 1% horse serum to the diluent (Table 3). Antiserum to broth- inoculated control animals has been shown previously to be unreactive in the ELISA (10).…”

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confidence: 96%

Identification of cross-reactive antigens between Mycoplasma pulmonis and Mycoplasma arthritidis

Minion¹,

Brown²,

Cassell³

1984

Infect Immun

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Serological cross-reactivity between Mycoplasma pulmonis and Mycoplasma arthriditis was investigated by enzyme-linked immunosorbent assay, immunoanalysis of electrophoretic blots, and protein A immunoprecipitation reactions. The results demonstrate that one-way cross-reactivity was present in both hyperimmunized and naturally infected rats and that the predominant cross-reactive antigens were M. pulmonis surface proteins. Distinct immunoblot patterns were demonstrated for M. pulmonis and M. arthriditis, allowing differentiation of the two species. The response to M. arthriditis antigens during natural infections differed greatly from that during hyperimmunization. Evidence suggested that nonprotein antigens were major determinants eliciting the antibody response to this mycoplasma. * Corresponding author. polyacrylamide gels. The results indicate that cross-reactive antigens are recognized not only by mice, but also by rats and rabbits, and that at least some of the cross-reactive antigens are surface proteins. MATERIALS AND METHODS Microorganisms. M. pulmonis UAB5782C and M. arthritidis PG-6 (ATCC 19611) were used throughout this study. The parent strain of M. pulmonis UAB5782C was originally isolated from the lungs of a rat with respiratory mycoplasmosis. The isolate was cloned twice and identified as a pure culture by immunofluorescence by R. A

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confidence: 96%

Identification of cross-reactive antigens between Mycoplasma pulmonis and Mycoplasma arthritidis

Minion¹,

Brown²,

Cassell³

1984

Infect Immun

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“…In experiments with inbred and congenic strains of mice, it was demonstrated that toxicity and death induced by M. arthritidis were associated with the major histocompatibility complex (MHC) haplotypes expressed. Mice possessing the H-2k or H-2d haplotype were susceptible, whereas those expressing H-2b appeared to be more resistant (10). Further influences asserted by the MHC haplotype were on an ulcerative dermal coagulation necrosis upon subcutaneous injection of M. arthritidis (7) and a reactivity of mouse lymphocytes toward M. arthritidis supernatants (MAS) acting as a soluble T-cell mitogen (5,9).…”

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confidence: 99%

Strain differences in sensitivity of rats to Mycoplasma arthritidis ISR 1 infection are under multiple gene control

et al. 1990

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At least 5 female rats from each of 24 inbred (ACI, AS, BDIX, BH, BN, BS, BUF, DA, LE, LEW, MWF, OM, SPRD-Cu3, W-Krypt, and WKY), RTI congenic [BH.lL(LEW), LEW.lA(AVN), LEW.lC(WIST), LEW.lLV3(BH), LEW.lK(SHR), and LEW.1N(BN)], and F1 hybrid [(LEW x BN)F1, (LEW.1W x LEW.1A)F1, and (LEW x LEW.1W)F1] strains, representing eight independent major histocompatibility complex (MHC) haplotypes (a, b, c, dvl, k, 1, n, and u) and five related RTI haplotypes (avi, lvl, 1v3, uv2, and uv3), were inoculated intravenously with Mycoplasma arthritidis, and the severity of the polyarthritis that developed was determined by estimating arthritis scores and weight reductions. The 24 inbred, congenic, and F1 hybrid rat strains differed considerably in their sensitivity to infection with M. arthritidis and in the severity of the polyarthritis that they developed. Statistical evaluation showed that in the acute phase (days 1 to 42 after infection) as well as in the chronic phase (days 39 to 121 after infection) of the disease, the means of the arthritis scores for the strains form a continuous variation without significant interruptions, with the very sensitive LEW rats, the RTI congenic rats on LEW background, the F1 hybrids with LEW, and the MWF, BS, BH, and DA rats on one end and the resistant WKY, BUF, W-Krypt, LE, and OM rats on the other end. A continuous variation was also observed for the means of the growth rates. There were, however, no significant differences between the sensitive and the resistant rat strains in the antibody titers determined by complement fixation test and enzyme immunoassay. Heritabilities of arthritis scores were calculated for all strains (h2 = 0.39 to 0.62), for the RTI congenic strains (h2 = 0.04 to 0.14), and for several strains with identical MHC genes (h2 = 0.61 to 0.93). The results show that non-MHC genes are probably responsible for the sensitivity of rats to infection with M. arthritidis.Animals. Up to 5 female rats from each of 24 inbred (ACI/

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“…Pyrogenic exotoxins stimulate macrophages to produce mediators such as IL-1 and TNF and production of these mediators was induced by products of mycoplasma [17][18][19]. Mycoplasmas produce haemolysins and cytotoxic substances that affect rat, mouse and chicken embryos and foetal rat skin fibroblasts [20][21][22]. These toxic materials might act on cells of the immune system to induce cytokines such as macrophage deactivating factor (MDF) or TGF-/3 resulting in suppression of macrophage antimicrobial activity that would account for the survival of mycoplasma.…”

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confidence: 99%

The effect of Mycoplasma arthritidis infection on the kinetics of colloidal carbon clearance in mice

Kaklamani

1993

FEMS Immunology and Medical Microbiology

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The activity of phagocytes from A/J mice was estimated by the carbon clearance test following injection of Mycoplasma arthritidis. Phagocytic activity was significantly depressed 12 h post-infection (P = 0.001) and returned to normal values at 24 h. For animals examined 2 and 7 days post-infection, the overall phagocytic activity increased significantly (P < 10(-4). Phagocytic activity gradually decreased and returned to that of the control group by the end of the fourth week. The relative weights of liver and spleen were significantly increased from the 2nd day post infection (P = 0.0028 and P = 0.0014 respectively) and remained increased until the end of the experiment. The early depressive effect on phagocytic activity may be related to superantigen activity with the production of mediators such as macrophage deactivating factor. The later expansion of the macrophage population might bring about the stimulation of autoreactive clones of T and B cells and be responsible for the chronic arthritis that developed in the mycoplasma treated mice.

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Toxicity but not arthritogenicity of Mycoplasma arthritidis for mice associates with the haplotype expressed at the major histocompatibility complex

Cited by 29 publications

References 14 publications

Identification of cross-reactive antigens between Mycoplasma pulmonis and Mycoplasma arthritidis

Identification of cross-reactive antigens between Mycoplasma pulmonis and Mycoplasma arthritidis

Strain differences in sensitivity of rats to Mycoplasma arthritidis ISR 1 infection are under multiple gene control

The effect of Mycoplasma arthritidis infection on the kinetics of colloidal carbon clearance in mice

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