Globally, 3 out of 5 persons lose their lives to chronic inflammatory conditions, such as diabetes, cardiovascular disorders, cancer, chronic respiratory diseases, skin diseases, renal diseases and obesity. Inflammatory diseases are the most prevailing cause of death worldwide and the numbers keep rising.
The network focuses on reducing the burden of infectious and inflammatory diseases caused by pathogens, damaged cells, toxic compounds or radiation in order to develop new diagnostic and treatment technologies.
As a society, we need more knowledge about the correlation between e.g. inflammation and development of cancer, about biomarkers and about molecular mechanisms of autoimmunity in e.g. rheumatological conditions - not to mention chronic mucosal inflammation. In the inflammation network we collaborate interdisciplinearily in order to find answers.
We comprise a wide range of researchers with interest in diagnostic methods, epidemiological data, inflammatory markers and intracellular pathways, understanding of cell population and tissue structures, among others.
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Paper of the Month
Marvin Werner
Bronchial asthma is a chronic inflammatory disease of the airways characterized by reversible bronchoconstriction. The pathophysiology involves various points, including bronchoconstriction, destruction of the epithelial layer and persistent inflammation, each of which has been well studied but whose interplay is not yet fully understood. Inflammation, which is partly triggered by allergic reactions, is one driving force behind bronchoconstriction. However, Bagley et al. now provide clear evidence that bronchoconstriction itself also contributes back to inflammation. In their work, published in Science, volume 384, they show how bronchoconstriction leads to inflammatory extrusion of epithelial cells which can be inhibited by gadolinium hexahydrate chloride or the peptide inhibitor GsMTx4. Bagley et al. thus provide a new basis for a mechano-inflammatory vicious cycle that directly links bronchospasm to the maintenance of inflammation. This work begins to close the loop in the pathogenesis of asthma and suggests new therapeutic targets for asthma treatment.
Bronchoconstriction damages airway epithelia by crowding-induced excess cell extrusion (science.org)
