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New mechanism identified as the cause of atherosclerosis in smokers

(Vienna, 19th September 2011) At the Congress of the International Society for the Prevention of Tobacco Induced Diseases in Vienna (21st to 23rd September) a new study shall be presented in which a previously unknown pathomechanism was identified which causes atherosclerosis through smoking. The MedUni Vienna was significantly involved in the study.

(Vienna, 19th September 2011) At the Congress of the International Society for the Prevention of Tobacco Induced Diseases in Vienna (21st to 23rd September) a new study shall be presented in which a previously unknown pathomechanism was identified which causes atherosclerosis through smoking. The MedUni Vienna was significantly involved in the study.
Simone Kreutmayer from the MedUni Innsbruck and co-first author Barbara Messner from the University Department of Surgery at the MedUni Vienna were able to show that smoking, in the form of “autoimmune hypothesis of atherosclerosis” causes vessel damage. Based on the new cell biological data it is likely that atherosclerosis caused by smoking is dependent on two factors: bacterial infections in childhood and stress for the vessel walls through smoking.

“Smoking sets in motion a mechanism which leads to the expression of auto-antigens on the vessel walls”, explains David Bernhard from the University Department of Surgery at Vienna General Hospital. Bernhard is both President of the “International Society for the Prevention of Tobacco Induced Diseases” and organiser of the Congress with participants from 21 countries, which shall be held at the MedUni Vienna from 21st to 23rd September.

Smoking stresses and leads to a harmful autoimmune reaction
The trigger of the damage is the heat shock protein 60, which actually has a repair and protective function in the cells. Infections during childhood through e.g. chlamydia or mycoplasma lead to the formation of anti-mycoplasma (or anti-chlamydia). The “vicious circle” of the autoimmune damage of the vessel walls begins after the vessel endothelium is stressed through the contents of smoke. The stress reaction of the endothelial cells leads to the heat shock protein 60 reaching the surface of the endothelial cells and being attacked there by autoreactive antibodies.

Bernhard says: “The study group led by Georg Wick from the Pathophysiology Department of the MedUni Innsbruck is currently working on a hyposensitisation approach in order to diminish this immune reaction, an approach which could also be successful in smokers. Above all, because no risk factor for atherosclerosis that has been examined to date triggers the heat shock protein 60 reaction in endothelial cells as greatly as smoking.”

The presentation of this study is only one highlight of the congress in Vienna. Amongst the others are lectures from renowned speakers such as David A. Scott and David Hein, both from the University of Louisville in Kentucky, a worldwide leading centre in the field of research regarding tobacco induced diseases. Scott’s lecture revolves around the interaction between smoking and the immune system and/or smoking and infections. Hein speaks about the genetic variability and risk of tumours in smokers.

The congress is to be opened by Health Minister Alois Stöger, and there are lectures from MedUni Vienna staff such as Ernest Groman from the Institute of Social Medicine (“Dehabituation programme in Austria”) and Manfred Neuberger from the Institute of Environmental Hygiene (“Futility of a partial smoking ban”) amongst others. Service: 9th Annual Conference of the International Society for the Prevention of Tobacco Induced Diseases 21st – 23rd September 2011, Jugendstilhörsaal, MedUni Vienna