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Research Summary

We are a translational research team, investigating the underlying disease mechanisms of obesity and cardiometabolic disease, with a special interest in inflammatory resolution.

Inflammation is a key driver of obesity-induced cardiometabolic pathophysiology. It is often forgotten that inflammation consists of two phases: the initial acute phase, followed by a resolving phase. In order for inflammation to subside, resolution must be actively induced by specialized pro-resolving lipid mediators (SPMs). These include the ω3-polyunsaturated fatty acids (PUFA)-derived protectins, resolvins and maresins, as well as the ω6-PUFA-derived LipoxinA4 (LXA4) and LipoxinB4 (LXB4). Lipoxins attenuate neutrophil recruitment and induce a pro-resolving M2 macrophage (MΦ) phenotype, which promotes efferocytosis, i.e. removal of apoptotic cells by phagocytes. LXA4 mediates protection mainly via the FPR2/ALX G-protein coupled receptor, while the LXB4 receptor is yet to be identified. Importantly, both ‘stop’ and ‘go’ signals are equally important for achieving adequate inflammatory response and any dysregulation may cause disease.

The overall aim of our research is to investigate and harness the therapeutic potential of lipoxins. Our studies suggest that treatment with lipoxins attenuates obesity-induced adipose inflammation and subsequent development of systemic disease (Börgeson et al, Cell Metabolism, 2015). We are currently investigating the underlying mechanisms that mediate this protection, and whether our results from preclinical models can be translated to human pathophysiology.

We combine experimental studies with clinical basic research to address our hypothesis in a translational manner. We use ex vivo cultures of tissue biopsies, which provide valuable "proof-of-principle" evidence to correlate our experimental data with human physiology. This translational approach requires state-of-the art experimental and clinical facilities, as well as a broad network of collaborators.



Page Manager: Mattias Lindgren|Last update: 6/26/2017

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