Role of the Porphyromonas gingivalis InlJ protein in homotypic and heterotypic biofilm development - PubMed (original) (raw)

Role of the Porphyromonas gingivalis InlJ protein in homotypic and heterotypic biofilm development

Cindy A Capestany et al. Infect Immun. 2006 May.

Abstract

The oral pathogen Porphyromonas gingivalis expresses a homolog of the internalin family protein InlJ. Inactivation of inlJ reduced monospecies biofilm formation by P. gingivalis. In contrast, heterotypic P. gingivalis-Streptococcus gordonii biofilm formation was enhanced in the InlJ-deficient mutant. The results indicate a nuanced role for InlJ in regulating biofilm accumulations of P. gingivalis.

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Figures

FIG. 1.

FIG. 1.

Microtiter plate monospecies biofilm production by P. gingivalis 33277 and the InlJ mutant at 24 h and 48 h. Asterisks indicate a significant difference (P < 0.05, t test; n = 3) between the mutant and parental strains. OD, optical density.

FIG. 2.

FIG. 2.

(A) Confocal laser scanning microscopy projections of monospecies biofilm formation by P. gingivalis strains 33277 and the InlJ mutant after 24 h. Magnification, ×40. (B) Total grain area analysis of a 268.6- by 268.6-μm x-y section. (C) Average biofilm height of P. gingivalis accumulation across three random x-z sections. Asterisks indicate a significant difference (P < 0.05, t test; n = 3) between the mutant and parental strains.

FIG. 3.

FIG. 3.

(A) Confocal laser scanning microscopy projections of mixed biofilms of S. gordonii DL1 with P. gingivalis strains 33277 and the InlJ mutant after 24 h. S. gordonii was prestained with hexidium iodide (red), and P. gingivalis was prestained with FITC (green). Magnification, ×40. (B) Total grain area analysis of a 268.6- × 268.6-μm x-y section. (C) Average biofilm height of P. gingivalis accumulation across three random x-z sections. Asterisks indicate a significant difference (P < 0.05, t test; n = 3) between the mutant and wild-type strains.

References

    1. Cabanes, D., P. Dehoux, O. Dussurget, L. Frangeul, and P. Cossart. 2002. Surface proteins and the pathogenic potential of Listeria monocytogenes. Trends Microbiol. 10**:**238-245. -PubMed
    1. Chen, W., K. E. Laidig, Y. Park, K. Park, J. R. Yates III, R. J. Lamont, and M. Hackett. 2001. Searching the Porphyromonas gingivalis genome with peptide fragmentation mass spectra. Analyst 126**:**52-57. -PubMed
    1. Cossart, P., J. Pizarro-Cerda, and M. Lecuit. 2003. Invasion of mammalian cells by Listeria monocytogenes: functional mimicry to subvert cellular functions. Trends Cell Biol. 13**:**23-31. -PubMed
    1. Heydorn, A., B. Ersboll, J. Kato, M. Hentzer, M. R. Parsek, T. Tolker-Nielsen, M. Givskov, and S. Molin. 2002. Statistical analysis of Pseudomonas aeruginosa biofilm development: impact of mutations in genes involved in twitching motility, cell-to-cell signaling, and stationary-phase sigma factor expression. Appl. Environ. Microbiol. 68**:**2008-2017. -PMC -PubMed
    1. Kajava, A. V. 1998. Structural diversity of leucine-rich repeat proteins. J. Mol. Biol. 277**:**519-527. -PubMed

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