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A hypothesis for the origin and pathogenesis of rheumatoid diseases.

Lorenz, W, Sigrist, G, Shakibaei, M, Mobasheri, A and Trautmann, C (2006) A hypothesis for the origin and pathogenesis of rheumatoid diseases. Rheumatol Int, 26 (7). pp. 641-654.

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It is well established that a correlation exists between rheumatoid arthritis (RA) and microbial damage. Material analyses have suggested that bacteria may be causative agents. This study was undertaken to further characterize the microbial agent responsible for pathogenesis of RA. In order to investigate whether substances in moist building materials can affect human cartilage, extracts from moist building materials were analysed for microbial components. Exposure of chondrocyte cultures to extracts in vitro showed that they were damaging the cultures. A direct correlation between strength of damage and concentration of MMP3 demonstrated that the effect was dose-dependent. High quantities of LPS were detected in the extracts. Experiments after deactivation with Polymyxin B showed that LPS are the causative agents. The present study leads to the hypothesis that LPS may bind to procollagen, as they bind to scavenger receptors. This procollagen endotoxin complex may block tropocollagen synthesis.

Item Type: Article
Divisions : Surrey research (other units)
Authors :
Lorenz, W
Sigrist, G
Shakibaei, M
Trautmann, C
Date : May 2006
DOI : 10.1007/s00296-005-0088-x
Uncontrolled Keywords : Air Pollution, Indoor, Arthritis, Rheumatoid, Bacteria, Blotting, Western, Cells, Cultured, Chondrocytes, Collagen Type II, Fungi, Humans, Lipopolysaccharides, Matrix Metalloproteinase 3, Polymyxin B
Related URLs :
Depositing User : Symplectic Elements
Date Deposited : 17 May 2017 10:12
Last Modified : 24 Jan 2020 18:43

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