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Departments of
*
Microbiology and
Pathology, Saga Medical School, Saga, Japan;
Department of Immunology and Microbiology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Tobetsu, Hokkaido, Japan; and
§
Research Team for Health Effects of Air Pollutants, National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan
We investigated whether oral administration of LPS exacerbated
collagen-induced arthritis (CIA) in mice, which was an experimental
model of autoimmune disease. CIA was induced by s.c. injection of type
II collagen emulsified with CFA into the base of the tail (day 0)
followed by a booster injection on day 21. To examine the ability of
LPS to exacerbate CIA, varying doses of LPS were orally administered on
day 50. The results showed that administration of LPS was followed by
reactivation of CIA in a dose-related fashion. Histologically, on day
55 there were marked edema of synovium proliferated by day 50, new
formation of fibrin, and intense infiltration of neutrophils
accompanied with a large number of mononuclear cells. Severe
destruction of cartilage and subchondral bone was also observed on day
70. The reactivation of CIA by oral administration of LPS was
associated with increase in anti-type II collagen IgG and IgG2a Abs as
well as varying kinds of cytokines including IL-12, IFN-
, IL-1ß,
and TNF-
. Polymyxin B sulfate given either orally or i.v. suppressed
the recurrence of CIA. Increased amounts of LPS were found in sera of
mice given the endotoxin orally. LPS from Salmonella
enteritidis, Salmonella typhimurium, and
Klebsiella pneumoniae and its component, lipid A from
Escherichia coli, also reactivated the disease. These
findings suggest that LPS from intestinal bacteria may play a role in
the exacerbation of autoimmune joint
inflammation.
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