ISSN: 0973-7510

E-ISSN: 2581-690X

Miroslav Pohanka1 and Oto Pavlis2
1Faculty of Military Health Sciences, University of Defense, Trebesska 1575, 50001 Hradec Kralove, Czech Republic.
2Centre of Biological Defense, 561 66 Techonin, Czech Republic.
J Pure Appl Microbiol. 2015;9(2):913-918
© The Author(s). 2015
Received: 04/01/2015 | Accepted: 09/02/2015 | Published: 30/06/2015

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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© The Author(s) 2015. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License which permits unrestricted use, sharing, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.