Caffeine is an alkaloid acting as an antagonist on adenosine receptors; however, the other targets for caffeine are known as well.Not much is known about effect of caffeine on immunity. In this work, we have hypothesized that caffeine can cause alteration of infectious disease progression. Tularemia, a zoonotic disease caused by Francisellatularensis, was used as the model disease and BALB/c mice were used as an in vivo model. Interleukines (IL) 1b, 2, 4, 6 and interferon g (IFN-g) were assayed by enzyme linked immuno-sorbent assay (ELISA) from plasma and bacterial burden was tested in spleen. We proved that caffeine caused increase of bacterial burden in the spleen in dose response manner. Oppose to this, IL-6 and IFN-gwere decreased in dose response manner. Caffeine seems to be able to modulate tularemia progression. Impact on neutrophils via adenosine receptors and on macrophages via cholinergic anti-inflammatory pathway is the most probable explanation.
Inflammation, Tularemia, Caffeine, Regulation, Adenosine receptor, Innate immunity, Acetylcholine, Cholinergic anti-inflammatory pathway
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