Previous studies have shown that type I diabetes (IDDM) increases the
risk of developing periodontitis by 2-3-fold. IDDM patients exhibit de
struction of the pancreatic beta cells, most probably caused by an aut
oimmune reaction. Evidence is accumulating to support the role of the
autoimmune response in periodontal pathogenesis. A cytokine, interleuk
in (IL)-10, has been reported to selectively promote the expansion of
a B lymphocyte lineage (CD5/LY1/B1) which has the propensity for secre
ting high levels of autoantibody. Therefore, the purpose of this proje
ct was to evaluate IL-10 production, percentage of CD5 B cells and the
frequency of anti-collagen secreting cells in peripheral blood mononu
clear cells of age, gender and race matched IDDM patients and controls
. IL-10 production was evaluated by an ELISA using the supernatant of
adherent peripheral blood cells cultured for 24 h in the presence of P
orphyromonas gingivalis lipopolysaccharide (LPS). In 8 of 31 patients,
IL-10 levels were significantly increased in IDDM compared to control
s and a higher percentage of CD5 B cells was also observed by flow cyt
ometry. In addition, these patients exhibited a higher frequency of an
ti-collagen secreting cells as elucidated by an ELISPOT. Moreover, tre
atment with a neutralizing anti-IL-10 antibody diminished the anti-col
lagen antibody response by 70%. These findings support the concept tha
t a subset of IDDM patients possess an extremely robust IL-10 response
following exposure to Gram-negative LPS, which could predispose them
to the development of periodontitis through a heightened autoimmune me
chanism.