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Infection and Immunity, March 2000, p. 1672-1680, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Complement Activation in Mycoplasma fermentans-Induced Mycoplasma Clearance from Infected Cells: Probing of the Organism with Monoclonal Antibodies against M161Ag

Satomi Kikkawa,1 Misako Matsumoto,1,2,* Tsuguo Sasaki,3 Miyuki Nishiguchi,1 Kazuhiko Tanaka,1 Kumao Toyoshima,1 and Tsukasa Seya1,2

Department of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Higashinari-ku, Osaka 537-8511,1 Department of General Biologics Control, National Institute of Health, Musashimurayama, Tokyo 208-0011,3 and Organization for Pharmaceutical Safety and Research, Tokyo 113,2 Japan

Received 13 September 1999/Returned for modification 29 October 1999/Accepted 25 November 1999

Mycoplasma fermentans, a cell wall-less prokaryote, is capable of infecting humans and has been suggested to serve as a cofactor in AIDS development. Recently, we discovered a novel lipoprotein with a molecular mass of 43 kDa originating from M. fermentans. This protein, named M161Ag, activated human complement via the alternative pathway and efficiently induced the proinflammatory cytokines interleukin 1beta (IL-1beta ), tumor necrosis factor alpha, IL-6, IL-10, and IL-12 in human peripheral blood monocytes. It is likely that M161Ag of M. fermentans affects the host immune system upon mycoplasma infection. In this study, we developed monoclonal antibodies (MAbs) against M161Ag and examined the direct role of complement in M. fermentans infection using these MAbs as probes. M. fermentans was rapidly cleared from the surfaces of infected cells by human complement, but a low-grade infection persisted in human tumor cell lines. Mycoplasma particles remaining alive in host cells may cause recurrent infection, and liberated M161Ag may serve as a biological response modifier affecting both innate and acquired immunity.

* Corresponding author. Mailing address: Department of Immunology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Higashinari-ku, Osaka 537-8511, Japan. Phone and fax: 81 6 6973 1209. E-mail: matsumoto{at}mail.mc.pret.osaka.jp.

Infection and Immunity, March 2000, p. 1672-1680, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Nishiguchi, M., Matsumoto, M., Takao, T., Hoshino, M., Shimonishi, Y., Tsuji, S., Begum, N. A., Takeuchi, O., Akira, S., Toyoshima, K., Seya, T. (2001). Mycoplasma fermentans Lipoprotein M161Ag-Induced Cell Activation Is Mediated by Toll-Like Receptor 2: Role of N-Terminal Hydrophobic Portion in its Multiple Functions. J. Immunol. 166: 2610-2616 [Abstract] [Full Text]  


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