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Infection and Immunity, March 2002, p. 1185-1192, Vol. 70, No. 3
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.3.1185-1192.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Modulation of Gamma Interferon-Induced Major Histocompatibility Complex Class II Gene Expression by Porphyromonas gingivalis Membrane Vesicles

Ratchapin Srisatjaluk, Girish J. Kotwal, Lawrence A. Hunt, and David E. Justus*

Department of Microbiology and Immunology, University of Louisville, Louisville, Kentucky 40292

Received 21 August 2001/ Returned for modification 9 October 2001/ Accepted 19 November 2001

Gamma interferon (IFN-{gamma})-induced endothelial cells actively participate in initiating immune responses by interacting with CD4+ T cells via class II major histocompatibility complex (MHC) surface glycoproteins. Previously, Porphyromonas gingivalis membrane vesicles were shown to selectively inhibit IFN-{gamma}-induced surface expression of HLA-DR molecules by human umbilical cord vascular endothelial cells. In this study, we demonstrated an absence of HLA-DR{alpha} mRNA from IFN-{gamma}-induced cells in the presence of P. gingivalis membrane vesicles by using reverse transcriptase-PCR and Southern blotting. Vesicles also prevented transcription of the gene encoding class II transactivator, a transactivator protein required for IFN-{gamma}-induced expression of MHC class II genes. In addition, the effects of vesicles on IFN-{gamma} signal transduction involving Jak and Stat proteins were characterized by using immunoprecipitation and Western blot analyses. Jak1 and Jak2 proteins could not be detected in endothelial cells treated with membrane vesicles. Consequently, IFN-{gamma}-induced phosphorylation of Jak1, Jak2, and Stat1{alpha} proteins was prevented. The class II-inhibitory effect of the membrane vesicles could be eliminated by heating vesicles at 100°C for 30 min or by treating them with a cysteine proteinase inhibitor. This indicates that the cysteine proteinases were most likely responsible for the absence of Jak proteins observed in vesicle-treated cells. The observed increased binding of radiolabeled IFN-{gamma} to vesicle-treated cells suggests that vesicles may also modulate the IFN-{gamma} interactions with the cell surface. However, no evidence was obtained demonstrating that vesicles affected the expression of IFN-{gamma} receptors. Thus, P. gingivalis membrane vesicles apparently inhibited IFN-{gamma}-induced MHC class II by disrupting the IFN-{gamma} signaling transduction pathway. Vesicle-inhibited class II expression also occurred in other IFN-{gamma}-inducible cells. This suggested that the ability of P. gingivalis membrane vesicles to modulate antigen presentation by key cells may be an important mechanism used by this particular bacterium to escape immunosurveillance, thereby favoring its colonization and invasion of host tissues.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Louisville, 319 Abraham Flexner Way, Louisville, KY 40202. Phone: (502) 852-5362. Fax: (502) 852-7531. E-mail: dejust01{at}gwise.louisville.edu.

Infection and Immunity, March 2002, p. 1185-1192, Vol. 70, No. 3
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.3.1185-1192.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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