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See Latest ArticlesHeavy metal exposure reverses genetic resistance to Chlamydia-induced arthritis
Arthritis Research & Therapy, 02/16/09
Inman RD et al. – Genetically defined cytokine production in the joint defines the severity of reactive arthritis by dictating the local clearance of the pathogen. This interplay can be dramatically altered by heavy metal exposure, which results in suppression of protective cytokines in the microenvironment of the joint.
Methods- Study examines an environmental toxin, mercuric chloride, as a modulator of experimental Chlamydia-induced arthritis resistance
- One group of rats received two sc injections of HgCl2 (1 mg/kg), 48 hrs apart
- 7 days later the animals received the intra-articular injection of synoviocyte-packaged Chlamydia
- Brown Norway (BN) rats receiving only Chlamydia had a minimal cellular infiltration in the joint, predominantly mononuclear cell in character
- In contrast, mercury-exposed rats had a marked exacerbation of the histopathological severity of the arthritis, infiltration was predominantly neutrophilic
- Mercury exposure was also associated with marked enhancement in IgE levels and in alteration in IgG2a/IgG1 ratio, reflecting a Th2 shift
- The local cytokine profile was markedly altered after mercury exposure; suppression of TNF-α, and IFN-γ, but an enhancement of VEGF
- This was associated with decreased host clearance capacity reflected in enhanced bacterial load in both the spleen and the joint
- This was accompanied by enhanced detection of microbial antigens in the synovial tissues
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