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Eva Särndahl

Befattning: Professor Organisation: Institutionen för medicinska vetenskaper

E-post: ZXZhLnNhcm5kYWhsO29ydS5zZQ==

Telefon: 019 303684

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Eva Särndahl

Om Eva Särndahl


The Role of Inflammasome Signaling in Health and Disease

Eva Särndahl is professor in Medical microbiology at Örebro University in Sweden. She has more than 25 years of experience in signal transduction involved in the regulation of the inflammatory process both in keeping immunological homeostasis but also during the development of inflammatory-mediated diseases. During the last seven years, the focus has been set on the involvement of inflammasome signaling in health and disease. Especially the role of dysregulated signaling due to variations in genes encoding the NLRP3 inflammasome in order to understand the inter-individual differences that determine why some individuals respond with severe, life-threatening inflammation, whereas others display a quiescent progression, or even remain asymptomatic following microbial challenge. Currently, this is investigated in patients with sepsis induced by S. aureus, E. coli and N. meningitides as well as in the development of type 2-diabetes and cardiovascular disease.

Besides its role in sensing microbes and their pathogen-associated molecular patterns (PAMPs), the NLRP3 inflammasome detects danger-associated molecular patterns (DAMPs), like nano particles, asbestos and silica but also endogenous substances. In collaboration, the underlying mechanisms in host innate response to stimuli and stressors are investigated in order to understand inflammatory-mediated diseases, including cystic fibrosis, auto-inflammatory/autoimmune diseases, inflammation developed in foundry workers and surgery-induced inflammation.

Short Career Narrative

I defended my thesis at Linköping University in 1994. My thesis revealed that chemotactic receptors are turned off by a lateral segregation between the receptor and its transducing partner, i.e. the G-protein; data that also suggests the cytoskeleton to function as a scaffold for signal transduction. Two years later I started my own research group studying the involvement of pro vs. anti-inflammatory signaling on leukocyte adhesion in order to understand the progression of inflammation and its resolution. During this time, I was the recipient of the Swedish Cancer Society 2-year postdoc position in 1995, and a 4-year Assisting Professorship by the Swedish Medical Research Council in 1998. In 2000-01, I was a Fulbright Scholar in Dr. Charles Serhan's laboratory at Harvard Medical School, USA studying and acquiring knowledge on the anti-inflammatory eicosanoid lipoxin. This work was awarded the national Crafoord research grant from the Royal Swedish Academy of Sciences.

In 2005, I was asked to join a project in which a rheumatologists and a geneticist needed help to understand the inflammatory mechanisms of a patient with auto-inflammatory symptoms. Polymorphisms of the NLRP3 inflammasome in combination with C10X in CARD8 were found to create an over-activated inflammasome resulting in elevated IL-1β production; thereby giving the patient his symptoms (Verma et al. 2008). The interest for inflammasome signaling was thereby uncovered, and has since been the main focus of my research. In 2007, got a professorship at Örebro University, and our research has been recognized by national founding as well as strategically research grants and positions from Örebro University. In 2013, the collaborative network “iRiSC - Inflammatory Response and Infection Susceptibility Centre” involving national and international researchers was launched with me as its Director. Read more about iRiSC.


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