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Katariina Öörni

Researcher at University of Helsinki

Publications -  116
Citations -  5369

Katariina Öörni is an academic researcher from University of Helsinki. The author has contributed to research in topics: Lipoprotein & Cholesterol. The author has an hindex of 32, co-authored 105 publications receiving 4373 citations. Previous affiliations of Katariina Öörni include University of California, Los Angeles & Sahlgrenska University Hospital.

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Journal ArticleDOI

Cholesterol Crystals Activate the NLRP3 Inflammasome in Human Macrophages: A Novel Link between Cholesterol Metabolism and Inflammation

Kristiina Rajamäki, +6 more
- 23 Jul 2010 - 
TL;DR: It is shown that human macrophages avidly phagocytose cholesterol crystals and store the ingested cholesterol as cholesteryl esters, and cholesterol crystals induced dose-dependent secretion of mature IL-1β from human monocytes and macrophage.
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Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities

Magnus Bäck, +4 more
- 01 Jul 2019 - 
TL;DR: In advanced atherosclerotic lesions, the ratio between specialized pro-resolving mediators and pro-inflammatory lipids is strikingly low, providing a molecular explanation for the defective inflammation resolution features of these lesions.
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Extracellular acidosis is a novel danger signal alerting innate immunity via the NLRP3 inflammasome

Kristiina Rajamäki, +6 more
- 10 May 2013 - 
TL;DR: The data suggest that acidic environment represents a novel endogenous danger signal alerting the innate immunity, and may contribute to inflammation in acidosis-associated pathologies such as atherosclerosis and post-ischemic inflammatory responses.
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Aggregation, fusion, and vesicle formation of modified low density lipoprotein particles: molecular mechanisms and effects on matrix interactions.

Katariina Öörni, +3 more
- 01 Nov 2000 - 
TL;DR: Molecular mechanisms that provide clues as to how aggregated lipid droplets and vesicles may be derived from modified LDL particles are discussed and how these modified forms of LDL, by means of their trapping to the extracellular matrix, may lead toextracellular lipid accumulation in the arterial intima.
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Serum Amyloid A Activates the NLRP3 Inflammasome via P2X7 Receptor and a Cathepsin B-Sensitive Pathway

Katri Niemi, +9 more
- 01 Jun 2011 - 
TL;DR: SAA can induce the expression of pro–IL-1β and activation of the NLRP3 inflammasome via P2X7 receptor and a cathepsin B-sensitive pathway and may promote the production of IL-1 β in tissues during systemic inflammation.