PI Soehnlein

Myeloid Cells in Vascular Inflammation and Therapy

Atherosclerosis is a chronic inflammatory disorder of large arteries. Following initial endothelial dysfunction, leukocytes start to infiltrate the arterial vessel wall contributing to lumen narrowing and ultimately to plaque rupture clinically evident as myocardial infarction or stroke. Bone marrow- and spleen-derived myeloid cells such as monocytes and neutrophils are crucially involved in atherogenesis, atheroprogression, and atherothrombosis. Our group focuses on recruitment of monocyte subsets and neutrophils to large arteries and on the investigation of pro-atherogenic mechanisms promoted by these cell types. 

 

Current themes:

Mechanisms of hypercholesterolemia-induced changes in leukocyte homeostasis

Functional responses of neutrophils in atherosclerosis

Damage-associated molecular patterns (DAMPs) during early processes of atherosclerosis

Mechanisms underlying neutrophil-mediated monocyte recruitment in atherosclerosis

 

Key publications:

  • Soehnlein O. The multiple roles of neutrophils in atherosclerosis.Circ Res, 2012;110:875-88.
  • Döring Y, Drechsler M, Vijayan S, Kemmerich K, Wantha S, Weber C, Gallo RL, Soehnlein O. Neutrophil-derived cathelicidin promotes atherosclerotic lesion formation.Circ Res, 2012;110:1052-6
  • Megens RTA, Vijayan S, Lievens D, Döring Y, Lutgens E, van Zandvoort M, Grommes J, Weber C, Soehnlein O. Presence of neutrophil extracellular traps in atherosclerotic lesions.Thromb Haemost, 2012; 107:597-8.
  • Grommes J, Alard JE, Drechsler M, Wantha S, Mörgelin M, Kuebler WM, Jacobs M, von Hundelshausen P, Markart P, Preissner KT, Hackeng TM, Koenen RR, Weber C, Soehnlein O. Disruption of platelet-derived chemokine heteromers abolishes endotoxin-induced lung injury.Am J Resp Crit Care Med, 2012;185:628-36.
  • Soehnlein O, Wantha S, Simsekyilmaz S, Döring Y, Megens RTA, Mause SF, Drechsler M, Smeets R, Weinandy S, Schreiber F, Gries T, Vijayan S, van Zandvoort MAMJ, Agerberth B, Pham CT, Gallo RL, Hackeng T, Liehn EA, Zernecke A, Klee D, Weber C, Neutrophil-derived cathelicidin protects from neointimal hyperplasia.Sci Transl Med, 2011; 3:103ra98.
  • Drechsler M, Megens RTA, van Zandvoort M, Weber C, Soehnlein O. Hyperlipidemia-triggered neutrophilia promotes early atherosclerosis.Circulation, 2010;122:1837-45.
  • Soehnlein O, Lindbom L. Phagocyte partnership during the onset and resolution of inflammation.Nat Rev Immunol. 2010;10:427-39.
  • Soehnlein O, Kai-Larsen Y, Frithiof R, Sorensen OE, Kenne E, Scharffetter-Kochanek K, Eriksson EE, Herwald H, Agerberth B, Lindbom L. Neutrophil primary granule proteins HBP and HNP1-3 boost bacterial phagocytosis by human and murine macrophages.J Clin Invest. 2008;118:3491-502.
  • Soehnlein O, Zernecke A, Eriksson EE, Rothfuchs AG, Pham CT, Herwald H, Bidzhekov K, Rottenberg ME, Weber C, Lindbom L. Neutrophil secretion products pave the way for inflammatory monocytes.Blood. 2008;112:1461-71.

 

Mitarbeiter:

group picture_II_scaled

Von links nach rechts: Oliver Soehnlein, MD, PhD; Jean-Eric Alard, PhD, post-doc; Patricia Lemnitzer, Lab tech; Henrick Friese, doctoral student; Claudia Geissler, Lab tech; Sarawuth Wantha, MSc, PhD student; Maik Drechsler, PhD, post-doc; Almudena Ortega-Gomez, PhD, post-doc; Helene Hartwig, MSc, PhD student; Jürgen Pyta, MSc, PhD student (mit Dr. Remco Megens); Klaus Kemmerich, MSc, PhD student.

 

Prinicpal Investigator:

PD Dr. Dr. med. Oliver Söhnlein

 
 
IPEKlogo

Direktor: Prof. Dr. med. Christian Weber

Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten (IPEK)

 

Pettenkoferstraße 8a & 9

80336 München

 

Tel.: 089-4400-54351

Fax: 089-4400-54352

Mail: Kreislaufinstitut@med.uni-muenchen.de

 

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