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Enzyme degradation and proinflammatory activity in arthritogenic and nonarthritogenic Eubacterium aerofaciens cell walls.

Abstract
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 A4alpha induces chronic arthritis in the rat after a single intraperitoneal injection, whereas CW of the other with PG type A4beta 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-alpha) 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-alpha 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.
AuthorsX Zhang, M Rimpiläinen, E Simelyte, P Toivanen
JournalInfection and immunity (Infect Immun) Vol. 69 Issue 12 Pg. 7277-84 (Dec 2001) ISSN: 0019-9567 [Print] United States
PMID11705898 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Chemokine CCL2
  • Muramic Acids
  • Peptidoglycan
  • Tumor Necrosis Factor-alpha
  • Muramidase
  • Endopeptidases
  • mutanolysin
Topics
  • Animals
  • Arthritis, Infectious (etiology)
  • Arthritis, Rheumatoid (etiology)
  • Carbohydrate Sequence
  • Cell Wall (immunology, metabolism)
  • Chemokine CCL2 (biosynthesis)
  • Digestive System (microbiology)
  • Endopeptidases (metabolism)
  • Eubacterium (classification, pathogenicity)
  • Gram-Positive Bacterial Infections (complications)
  • Liver (chemistry)
  • Macrophages, Peritoneal (immunology)
  • Molecular Sequence Data
  • Muramic Acids (analysis)
  • Muramidase (metabolism)
  • Peptidoglycan (immunology, metabolism)
  • Rats
  • Species Specificity
  • Spleen (chemistry)
  • Synovial Membrane (chemistry)
  • Tumor Necrosis Factor-alpha (biosynthesis)

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