Abstract
The role of infection in autoimmunity is widely discussed. In this Study we concentrated on relationship between Helicobacter pylori as a very important gastroduodenal pathogen and autoimmune thyroiditis (AT).
Forty seven AT patients and 34 healthy controls were enrolled. They were split into: THP (H. pylori positive patients, n = 17), THN (H. pylori negative patients, n = 30), CP (H. pylori positive controls, n = 17) and CN groups (H.pylori negative controls, n=17).
By protein microarray we analysed production of 23 cytokines and chemokines prior and post stimulation with H.pylori lysate and its lipopolysacharide (LPS). Reactivity to lysate as well as to bacterial LPS differed within groups.
The lowest basal cytokine and chemokine production was observed in CN group but these subjects reacted significantly to specific stimulation by increasing IFN-gamma (in comparison with THP p=0.01 for LPS and p=0.004 for H. pylori lysate) and TGFbeta production (p=0.015 for LIPS). In contrast, IL-10 and IL-5 were decreased in this group.
In CP, THN and THP groups, we observed in general higher chemokine response. THP group increased proinflammatory IL-6 after specific stimulation as well (in comparison with CP p < 0.0001 for LPS stimulation).
We observed different "reactivity pattern" to H. pylori within groups with low basal cytokine and chemokine production in healthy H.pylori negative controls but with clear specific response in IFN-gamma and TGF-beta production in this group. Adequate immune reaction which is joined to appropriate immunoregulation leads to prevention of the chronic infection and on the other hand may prevent the development of "connected" diseases such as autoimmune.