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Infection and Immunity, January 2005, p. 245-249, Vol. 73, No. 1
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.1.245-249.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Association of a Major Protein Antigen of Mycoplasma arthritidis with Virulence

A.-H. T. Tu,1 B. Clapper,2 T. R. Schoeb,1 A. Elgavish,1 J. Zhang,1 L. Liu,1,{dagger} H. Yu,1 and K. Dybvig1,2*

Department of Genetics,1 Microbiology, University of Alabama at Birmingham, Birmingham, Alabama2

Received 9 July 2004/ Returned for modification 13 August 2004/ Accepted 17 September 2004

Mycoplasma arthritidis causes acute polyarthritis in rats and chronic proliferative arthritis in mice. M. arthritidis-induced arthritis serves as a model for arthritis caused by infectious agents and as a model for examining the role of the superantigen MAM (M. arthritidis T-cell mitogen) in the development of autoimmunity. M. arthritidis strain 158-1 is a spontaneous mutant of strain 158 that has a drastic reduction in virulence. We show that the mutant is missing a major antigen of 47 kDa (P47) and has acquired a protein of 67 kDa (P67). P47 and P67 partitioned into the detergent phase by extraction with Triton X-114. Coomassie blue staining of sodium dodecyl sulfate-polyacrylamide gels show that P67 is produced in abundance. Analysis of gel-purified P67 by mass spectrometry led to its identification as a lipoprotein (the open reading frame [ORF] 619 gene product) predicted from the genome sequence of M. arthritidis. PCR analysis of genomic DNA from 158 and 158-1 indicates that P47 and P67 are encoded by the same ORF 619 gene and differ only in the number of repeats in a tandem repeat region. By two-dimensional polyacrylamide gel analysis, no protein differences were detectable between 158 and 158-1 other than P47 and P67. Collectively, the data suggest that the tandem repeat region of P47 and P67 influences disease outcome.

* Corresponding author. Mailing address: Department of Genetics, KAUL, Room 720, University of Alabama at Birmingham, Birmingham, AL 35294-0024. Phone: (205) 934-9327. Fax: (205) 975-4418. E-mail: dybvig{at}uab.edu.

Editor: J. T. Barbieri

{dagger} Present address: National Institute of Allergy and Infectious Diseases, National Institutes of Health, Laboratory of Host Defenses, Bethesda, MD 20892.

Infection and Immunity, January 2005, p. 245-249, Vol. 73, No. 1
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.1.245-249.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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