Behçet's disease patients present high levels of deglycosylated anti-lipoteichoic acid IgG and high IL-8 production after lipoteichoic acid stimulation.

Journal Article

OBJECTIVES: Lipoteichoic acid (LTA), induces some of the clinical symptoms of Behçet's disease (BD) in a rat animal model. These results led to the hypothesis that LTA may also trigger BD in humans. We investigated the humoral and cellular immune response against LTA and lipopolysaccharide (LPS) in patients with BD, and compared these responses with those of patients with active chronic oral ulcers (OU) and normal controls. METHODS: Samples were obtained from 12 active BD, 12 inactive BD, 12 active OU and 12 normal controls. Anti-LTA, anti-LPS antibodies levels and the capacity of immune complexes anti-LTA IgG-LTA to activate complement were studied. Exposed mannose residues in anti-LTA IgG were analyzed in the four groups. The interleukin-8 (IL-8) production by peripheral blood mononuclear cells cultures after LTA and LPS stimulation was also studied in all groups. RESULTS: The capacity to bind mannan binding protein (MBP) of anti-LTA IgGs was significantly higher in BD and active OU patients relative to normal controls (p < 0.001). However, only active BD patients generated significantly higher levels of C5a than controls (p < 0.0001). The IgGs purified from the sera of BD patients showed a high specificity for LTA from Streptococcus sanguis or Streptococcus faecalis. LTA also stimulates the secretion of IL-8 in peripheral blood mononuclear cells isolated from active BD patients. Anti-LPS IgA and IgG titers were significantly higher only in active OU patients relative to normal controls (p < 0.0018). CONCLUSION: These results suggest a mechanism involving LTA from streptococci in the pathogenesis of BD.

Full Text

Duke Authors

Cited Authors

  • Cuchacovich, M; Merino, G; Yamamoto, JH; Villarroel, F; Saavedra, T; Jofre, S; Gatica, H; Velasquez, V; Pizzo, SV; Gonzalez-Gronow, M

Published Date

  • July 2005

Published In

Volume / Issue

  • 23 / 4 Suppl 38

Start / End Page

  • S27 - S34

PubMed ID

  • 16273761

International Standard Serial Number (ISSN)

  • 0392-856X

Language

  • eng

Conference Location

  • Italy