Publications by authors named "H-E Claesson"

Article Synopsis
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) work by inhibiting enzymes involved in the production of proinflammatory compounds like prostaglandins and leukotrienes, impacting two types of macrophages: proinflammatory M1 and proresolving M2.
  • The study utilized advanced mass spectrometry to analyze lipid mediator profiles, revealing that different inhibitors affect inflammatory responses differently in M1 and M2 macrophages.
  • Findings suggest that targeting specific enzymes in lipid biosynthesis can significantly influence the lipid profiles of macrophages, potentially improving treatment strategies for inflammatory diseases.
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Dendritic cells (DCs) involved in proinflammatory immune responses derive mainly from peripheral monocytes, and the cells subsequently mature and migrate into the inflammatory micromilieu. Here we report that suppressing of 15-lipoxygenase-1 led to a substantial reduction in DC spreading and podosome formation in vitro. The surface expression of CD83 was significantly lower in both sh-15-lipoxygenase-1 (15-LOX-1)-transduced cells and DCs cultivated in the presence of a novel specific 15-LOX-1 inhibitor.

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Human eosinophils contain abundant amounts of 15-lipoxygenase (LO)-1. The biological role of 15-LO-1 in humans, however, is unclear. Incubation of eosinophils with arachidonic acid led to formation of a product with a UV absorbance maximum at 282 nm and shorter retention time than leukotriene (LT)C4 in reverse-phase HPLC.

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A technique is described in which sheets of corneal endothelium are removed from human donor corneo-scleral discs. Celloidin solution was applied to the endothelial surface, allowed to dry, peeled off with the attached endothelial cell layer and mounted on a glass slide. Following removal of the celloidin with acetone, this endothelial cell flat mount was then stained with H&E and monoclonal antibodies to cell adhesion molecules.

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Arachidonic acid and prostaglandin H2 elevate the levels of adenosine 3':5'-monophosphate (cyclic AMP) in Balb/c 3T3 fibroblasts. This effect was inhibited by 15-hydroperoxy-5,8,11,13-eicosatetraenoic acid, an inhibitor of prostaglandin I2 synthase (Claesson, H.-E.

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Prostaglandins (PG)E1, E2 and I2 were produced by polyoma virus transformed (py) 3T3 fibroblasts. The levels of PGE1, PGE2 and 6-keto-PGF1 alpha (degradation product of PGI2) were 22.7, 225 and 33.

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