Background: Evidence is emerging that molecular chaperones, in addition to their intracellular protein folding actions, can act as intercellular signaling proteins with an ability to modulate leukocyte function. Recent evidence has also shown that these proteins can exist in the circulation and may be involved in disease pathogenesis. We have used periodontitis and its treatment as a model of inflammation in the human to determine its effects on levels of circulating HSP10, HSP60 and BiP.
Methodology/principal findings: A group of periodontal patients and matched controls were examined at the beginning of the study and then at 1 day and 6 months following periodontal or control therapy. Plasma levels of HSP10, HSP60 and BiP were measured by immunoassay and related to other plasma measures of inflammation. Periodontal patients had significantly less circulating levels of HSP10 or BiP compared with the controls. In contrast, more periodontal patients had intermediate levels of HSP60. Treatment of the periodontitis caused an increase in plasma levels of HSP10 although it had no effect on BiP. Treatment had no influence of HSP60 levels. Plasma HSP10 levels after therapy correlated with markers of periodontal clinical improvement.
Conclusions/significance: Circulating levels of molecular chaperones are influenced by local inflammation. HSP10 is known to be an anti-inflammatory factor. The marked decrease of this circulating protein in active inflammation and its recovery post-treatment suggests that it may have a role in controlling periodontal inflammation.