Microvascular physiology

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Our research activities are focused on vascular and immune cell interactions in inflammation, and on signaling functions of specific gene products and metabolic factors in the regulation of immune cell trafficking and vessel wall function in the inflammatory process.

The inflammatory reaction constitutes the first line of defense against noxious stimuli, and represents the initial phase in the healing process following tissue injury. Adaptation of vascular function at the microcirculatory level and recruitment of circulating white blood cells are key factors in the protective immune response. However, inflammation may itself cause harm to the host and result in tissue damage and organ dysfunction. A misdirected or inappropriately triggered inflammatory response underlies many of our common diseases like allergy/asthma, atherosclerosis, and autoimmune diseases, in which situations activation of circulating leukocytes and dysregulation of vascular function are considered to play central roles in the disease development.

Group members

Ellinor KennePostdoc
Erik LundebergPhD student
Joel RasmusonPhD student
Karl-E ArforsSenior researcher
Lennart LindbomProfessor


Through a multidisciplinary methodological approach we aim at advancing our understanding of mechanisms regulating leukocyte recruitment and endothelial barrier function in inflammation, and to explore potential new targets for intervention in inflammatory disease processes.

Our laboratory hosts intravital microscopy and whole-organ animal models enabling detailed characterization of dynamic vascular and immune cell responses in living tissue; confocal microscopy and FACS-analysis for detection of signal transduction events; cell culture methodology and migration assays for analysis of cell-cell and cell-matrix interactions.

Selected publications

Induction of the human cathelicidin LL-37 as a novel treatment against bacterial infections.
van der Does A, Bergman P, Agerberth B, Lindbom L
J. Leukoc. Biol. 2012 Oct;92(4):735-42

Phagocyte partnership during the onset and resolution of inflammation.
Soehnlein O, Lindbom L
Nat. Rev. Immunol. 2010 Jun;10(6):427-39

Distinct infiltration of neutrophils in lesion shoulders in ApoE-/- mice.
Rotzius P, Thams S, Soehnlein O, Kenne E, Tseng C, Björkström N, et al
Am. J. Pathol. 2010 Jul;177(1):493-500

Leukotriene B4-induced changes in vascular permeability are mediated by neutrophil release of heparin-binding protein (HBP/CAP37/azurocidin).
Di Gennaro A, Kenne E, Wan M, Soehnlein O, Lindbom L, Haeggström J
FASEB J. 2009 Jun;23(6):1750-7

Neutrophil primary granule proteins HBP and HNP1-3 boost bacterial phagocytosis by human and murine macrophages.
Soehnlein O, Kai-Larsen Y, Frithiof R, Sorensen O, Kenne E, Scharffetter-Kochanek K, et al
J. Clin. Invest. 2008 Oct;118(10):3491-502 

Neutrophil secretion products pave the way for inflammatory monocytes.
Soehnlein O, Zernecke A, Eriksson E, Rothfuchs A, Pham C, Herwald H, et al
Blood 2008 Aug;112(4):1461-71

M protein, a classical bacterial virulence determinant, forms complexes with fibrinogen that induce vascular leakage.
Herwald H, Cramer H, Mörgelin M, Russell W, Sollenberg U, Norrby-Teglund A, et al
Cell 2004 Feb;116(3):367-79

Heparin-binding protein (HBP/CAP37): a missing link in neutrophil-evoked alteration of vascular permeability.
Gautam N, Olofsson A, Herwald H, Iversen L, Lundgren-Akerlund E, Hedqvist P, et al
Nat. Med. 2001 Oct;7(10):1123-7

Importance of primary capture and L-selectin-dependent secondary capture in leukocyte accumulation in inflammation and atherosclerosis in vivo.
Eriksson E, Xie X, Werr J, Thoren P, Lindbom L
J. Exp. Med. 2001 Jul;194(2):205-18

Signaling via beta(2) integrins triggers neutrophil-dependent alteration in endothelial barrier function.
Gautam N, Herwald H, Hedqvist P, Lindbom L
J. Exp. Med. 2000 Jun;191(11):1829-39

Contact us 


Lennart Lindbom

Phone: 08-524 872 07
Organizational unit: Lindbom Lennart group - Microvascular Physiology
E-mail: Lennart.Lindbom@ki.se