Increased proliferative response of peripheral blood mononuclear cells and T cells to Streptococcus mutans and glucosyltransferase D antigens in the exacerbation stage of recurrent aphthous ulcerations.

نویسندگان

  • Andy Sun
  • Jean-San Chia
  • Chun-Pin Chiang
چکیده

BACKGROUND AND PURPOSE Cytotoxic T lymphocyte-induced lysis of virus-infected oral epithelial cells has been shown to be a cause of early ulcer formation in recurrent aphthous ulcerations (RAU). To test whether bacteria and their associated antigens are involved in the disease process of RAU, the proliferative response (PR) to different streptococcal species in peripheral blood mononuclear cells (PBMC) and T cells isolated from RAU patients at the exacerbation stage was determined. METHODS PBMC and T cells were isolated from 39 patients with RAU, 21 patients with erosive oral lichen plaus (EOLP, disease control group), and 22 healthy subjects (normal control group). Streptococcus mutans, Streptococcus sanguis, Streptococcus oralis, Streptococcus gordonii, Streptococcus mitis and their associated antigen, glucosyltransferase D (GtfD), were used to stimulate isolated PBMC and T cells in in vitro proliferation assays. RESULTS PBMC and T cells isolated from RAU patients at the exacerbation stage showed a significantly higher PR to S. mutans antigen and GtfD than those isolated from EOLP patients or healthy control subjects (p < 0.05). GtfD was a more potent stimulation antigen than S. mutans. However, elevated PRs to S. mutans antigen and GtfD were transient and present only in the exacerbation stage of RAU. These elevated PRs declined to normal levels in the postexacerbation and convalescence stages of RAU. Furthermore, the GtfD-stimulated PR in PBMC and T cells was correlated with the severity of RAU. CONCLUSION In addition to viral infections, streptococci and their associated antigen, GtfD, may be involved in the disease process of RAU, especially in the exacerbation stage.

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عنوان ژورنال:
  • Journal of the Formosan Medical Association = Taiwan yi zhi

دوره 101 8  شماره 

صفحات  -

تاریخ انتشار 2002