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Infection and Immunity, December 2001, p. 7277-7284, Vol. 69, No. 12
Department of Medical Microbiology, Turku
Immunology Center, University of Turku, Turku, Finland
Received 4 June 2001/Returned for modification 7 August
2001/Accepted 4 September 2001
Two almost-identical strains of Eubacterium
aerofaciens isolated from the normal human gut flora were used.
The cell wall (CW) of one strain with a peptidoglycan (PG) type A4
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.12.7277-7284.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Enzyme Degradation and Proinflammatory Activity in
Arthritogenic and Nonarthritogenic Eubacterium
aerofaciens Cell Walls
imelyte, and
induces chronic arthritis in the rat after a single intraperitoneal
injection, whereas CW of the other with PG type A4
induces only a
transient acute arthritis. The CW of the arthritogenic E.
aerofaciens was a twofold-more-potent stimulator of the
proinflammatory cytokines tumor necrosis factor alpha (TNF-
) and
monocyte chemoattractant protein 1 (MCP-1) than the nonarthritogenic
CW. After degradation with mutanolysin, the capacity of the
arthritogenic PG to stimulate production of TNF-
and MCP-1 was
significantly increased, whereas that of the nonarthritogenic PG was
significantly decreased. In other words, after enzyme degradation the
arthritogenic PG had a four- to fivefold-stronger stimulatory capacity
than that of the enzyme-treated nonarthritogenic PG. These findings
indicate that the arthritogenicity of CW or a PG is not dependent on
the enzyme resistance alone but also on how the PG fragments released by enzyme degradation stimulate the production of proinflammatory cytokines.
*
Corresponding author. Mailing address: Department of
Medical Microbiology, University of Turku, Kiinamyllynkatu 13, FIN-20520 Turku, Finland. Phone: 358-2-333-7405. Fax: 358-2-233-0008. E-mail: xzhang{at}utu.fi.
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