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News / Press Releases

PRESS RELEASE

Lausanne, 18 May 2008. MUGEN partner Dr. J. Tschopp and his group provide key molecular insights into how airborne pollutants, including asbestos and silica, lead to inflammation, pulmonary diseases and pottentially lung cancer and fibrosis. 

(view full press release) 



PRESS RELEASE

Athens, 6  May 2008. Using a unique murine model for human Crohn's disease, MUGEN's NoE participants [G. Kollias, D. Kontoyiannis (Fleming), W. Müller (HZI), B. Malissen (CNRS]) identified key molecules that control T lymphocyte migration to the small intestine. Their discovery brings into focus the use of novel, more efficient therapeutic approaches against Crohn's disease.

(view full press release)



PRESS RELEASE

Lausanne, 12  March 2008. MUGEN participant Professor Jurg Tschopp and his colleagues have reported that activation of the inflammasome, a multi-protein complex involved in the innate immune response against many pathogens, is also important for the generation of an effective inflammatory response to adenoviruses and other DNA viruses.

(view full press release)



PRESS RELEASE

Schlieren, 25 April 2007. MUGEN participant Cytos Biotechnology enters exclusive license agreement with Novartis to develop, manufacture and commercialize novel vaccine for treatment of nicotine addiction.

(view full press release)



PRESS RELEASE

Athens, 29 March 2007. MUGEN participant Professor Manolis Pasparakis and his colleagues have identified molecular basis of inflammatory bowel disease.

The study, which is published in the March 2007 issue of the Nature, shows that blocking a signalling molecule causes severe intestinal inflammation in mice and reveals a molecular mechanism that is likely to also underpin human inflammatory bowel disease. (view full press release)



PRESS RELEASE

Athens, 4 January 2007. MUGEN partner BSRC “Alexander Fleming” has recently published at PLoS One (PDF) the article entitled “Soluble TNF Mediates the Transition from Pulmonary Inflammation to Fibrosis”.


Soluble TNF Mediates the Transition from Pulmonary Inflammation to Fibrosis

Researchers from the Institute of Immunology at BSRC Alexander Fleming revealed that soluble TNF driven pulmonary inflammation is among the primary pathogenetic mechanisms leading to the development of pulmonary fibrosis. The study, published in PLoS One (2006, 1(1):e108) (PDF), indicates a primary detrimental role of soluble TNF in the pathological cascade, separating it from the beneficial role of transmembrane TNF. Most importantly, it suggests the importance of assessing the efficacy of soluble TNF antagonists in the treatment of Idiopathic Pulmonary Fibrosis, a lethal, incurable pulmonary disease.



PRESS RELEASE

Lund, 6 November 2006. MUGEN participant Prof. Rikard Holmdahl and his colleagues have recently published at PLoS Medicine (PDF) the article entitled “A New Arthritis Therapy with Oxidative Burst Inducers”.


A New Arthritis Therapy with Oxidative Burst Inducers

Oxygen radicals, that until now have been regarded to be extremely toxic, could act therapeutic against rheumatoid arthritis. The finding, discovered by a research group in Lund, Sweden, is now supported by extensive animal experiments.

Experiments in rats shows that a substance that increases the production of free oxygen radicals decrease the rheumatic symptoms with an efficacy at least as good as therapies used for arthritis today. A mildly speaking radical new method to treat rheumatoid arthritis, and possibly also other so called autoimmune diseases such as MS, has occupied a research group led by Professor Rikard Holmdahl for many years. Via investigations of genetically modified rats and mice they have discovered truths arguing against established medical dogmas. Could the toxic free oxygen radicals that are produced when oxygen are turned over in the body maybe play a positive role in the battle against the inflammatory process that causes arthritis?

In August this year the group published the biological background for the theory in PNAS. In the internet-based journal PLoS Medicine (View PDF) they now take one step further. They have tested to administrate a substance with a capacity to make cells in the immune-defense to produce free oxygen radicals in genetically modified rats, among those rats with symptoms of arthritis. They selected the substance Phytol, present in chlorophyll and used in the production of vitamin E.
-We could see that Phytol increased the production of free oxygen radicals, says Malin Hultqvist, a member of the Medical Inflammation Research group at Lund’s University, Sweden.

Continued investigations reveled that the increased production of free radicals produced could both prevent the onset of arthritis and ameliorate already established symptoms. According to the report the treatment was as effective as therapies for arthritis used today including the novel TNF-a blockers.
-The explanation for this phenomenon is most likely that a delicate balance is affected, explains Rikard Holmdahl. Free radicals are needed in the immune-defense to kill threatening agents such as bacteria and for the immune system to work. If the radical production is decreased the balance is altered and a damaging process could initiate.
-It is known that the therapies for rheumatoid arthritis on the market today do not help all patients, says Malin Hultqvist. There is therefore a need for further alternatives. The research is still on an early stage and a lot of work is still needed, not least to determine the side effects of the treatment.

 

Articles
1. Introducing MUGEN 25-08-2005. Functional Genomics in Mutant Mouse Models as Tools to Investigate the Complexity of Human Immunological Disease...
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