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Suppression of inflammatory gene expression in T cells by Porphyromonas gingivalis is mediated by targeting MAPK

Hazem Khalaf1, Isak Demirel, Torbjörn Bengtsson

  • 1Division of Clinical Medicine, School of Health and Medical Sciences, Örebro University, Örebro, Sweden

Cellular & Molecular Immunology
|July 30, 2013
PubMed

Insights

Porphyromonas gingivalis suppresses inflammatory gene expression by inhibiting T-cell signaling pathways. This bacterium targets mitogen-activated protein kinase (MAPK) pathways, affecting immune responses.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Porphyromonas gingivalis is known to impact host immune responses.
  • Previous research indicated degradation of cytokines and chemokines by bacterial cysteine proteinases.
  • Mechanisms of P. gingivalis in altering intracellular signaling, proliferation, and inflammation remain unclear.

Purpose of the Study:

  • To investigate the effects of P. gingivalis on Jurkat T-cell signal transduction.
  • To analyze the impact on Interleukin-2 (IL-2) and CXCL8 gene expression.
  • To elucidate the specific intracellular signaling pathways affected by P. gingivalis.

Main Methods:

  • Analysis of gene expression levels for IL-2 and CXCL8 in Jurkat T-cells treated with P. gingivalis.
  • Western blot analysis to assess the phosphorylation status of key signaling proteins, including protein kinase C (PKC) and p38.
  • Examination of intracellular signaling pathways such as activator protein-1 (AP-1), NFκB, NFAT, STAT5, and mitogen-activated protein kinases (MAPKs).

Main Results:

  • Viable P. gingivalis significantly suppressed CXCL8 gene expression, but not IL-2.
  • P. gingivalis inhibited the expression of c-Jun and c-Fos, key components of AP-1, without affecting NFκB, NFAT, or STAT5.
  • The bacterium prevented phosphorylation of PKC and p38, crucial steps in MAPK signaling, and decreased SOCS1 and SOCS3 expression.

Conclusions:

  • P. gingivalis suppresses inflammatory gene expression by targeting MAPK pathways in T cells.
  • The bacterium's mechanism involves inhibiting PKC and p38 phosphorylation, thereby modulating T-cell responses.
  • These findings provide insight into how P. gingivalis manipulates host immune signaling.

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