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.
Acute kidney injury (AKI) is defined by an abrupt decrease in renal function. The incidence of AKI varies from 5% in all hospitalized patients to 30-50% in intensive care units. Most interventional trails in AKI have failed in humans so there is a need for better therapeutic approaches to prevent or treat AKI.
There is an increasing evidence for an important role for the innate immune cells in propagation of AKI. Following acute injury to the kidney, macrophages plan an important role in recovery of functional and structural integrity, but renal fibrosis and progressive functional decline occur with incomplete recovery
This paper described a novel mechanism by which prostaglandins modulate macrophage phenotype following AKI and provide new insight into mechanisms underlying detrimental kidney effects of non-steroidal anti-inflammatory (NSAID) drugs that inhibit cyclooxygenase activity.