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Anna Karlsson-Bengtsson

Professor

Anna Karlsson-Bengtsson
Professor
anna.karlsson@gu.se
0708-187634

Postal Address: Box 480, 40530 Göteborg
Visiting Address: Guldhedsgatan 10 A, plan 2 , 41346 Göteborg


Department of Rheumatology a Inflammation Research at Institute of Medicine (More Information)
Box 480
405 30 Göteborg
0313421000
Fax: +46 31823925
Visiting Address: Medicinaregatan 3, plan 5 , 413 90 Göteborg

About Anna Karlsson-Bengtsson

My basic training in Chemistry was done att Linköping University, where I also began my PhD studies. During my education, I moved to the Department of Medical Microbiology and Immunology at the University of Gothenburg and received my PhD in 1996. Since 2004 I hold a professorship in Experimental Rheumatology at the Department of Rheumatology and Inflammation Research, Institute of Medicine.

My special research interest encompass how the inflammatory process is regulated, focusing on the function of phagocytizing white blood cells and their interaction with galectins, a group of endogenous lectins that appears to be partaking in many important biological processes, e.g., cell differentiation, cancer development, immune functions, and, inflammation.

Research

Galectins - Novel Activators of Neutrophil Function and Modulators of Inflammatory Diseases

Phagocytosing white blood cells (neutrophils, monocytes/ macrophages) are of central importance for our defense against infection, but the mechanisms responsible for bacterial killing may damage also endogenous, healthy tissue. Hence, proper modulation of phagocyte function during inflammatory processes is of outmost importance to minimize collateral damage while optimizing threat erradication.

The aim of our research is to study the interaction between phagocytes, especially neutrophils, and a novel group of inflammatory mediators, the galectins. Members of the galectin family are currently being established as important inflammatory modulators with pronounced, but sometimes contradictory, effects; e.g., they can induce massive production of reactive oxygen species (ROS) in neutrophils and at the same time dampen the development of septic arthritis (see below). By studying the interaction between phagocytes and galectins, we want to increase our understanding of how phagocyte function is regulated on a molecular level and how galectins thereby affect the outcome of in vivo inflammatory processes. We have reported that galectin-1, -3 and -8 are potent activators of the human neutrophil respiratory burst, provided that the cells first have experienced the process of extravasation. The basis for this ”priming” appears to be the upregulation of cell surface receptors from intracellular granules.

We now continue our investigations on the galectin – neutrophil interaction by searching for activating galectin receptors, studying synthesis, sorting and secretion of endogenous galectin, defining the molecular mechanisms behind a the priming pathways and exploring the role of galectins in neutrophil apoptosis and clearance. We combine these in vitro experimental studies of molecules, cells, and tissues with in vivo studies of galectins in inflammatory situations, exploring the role of galectin-3 in murine models of neonatal brain injury after asphyxia, septic arthritis, and antibody-induced arthritis, including disease development in galectin-3 deficient animals. We also collaborate with clinical researchers in studies of patients suffering from acute injury or chronic inflammatory disease.

We base our work on the following hypotheses:

  • Galectins, especially galectin-3, take part in the inflammatory process by activation of neutrophils, and may be a disease marker in acute and chronic inflammatory settings.
  • Neutrophil responsiveness to galectins is highly regulated by the cell’s ability to become primed, a characteristic that is of decisive importance for balanced execution of cellular functions during an inflammatory process.


Ourspecific aims are:

  • to reveal the receptors, signal transduction pathways and functional outcomes of galectin-induced neutrophil activation,
  • to study the basic mechanisms of galectin-3 synthesis, sorting, and secretion in neutrophils,
  • to clarify the molecular mechanisms behind the process of neutrophil priming leading to responsiveness to galectins, and
  • to study the role of galectins in the development of acute inflammatory tissue damage as well as in conditions of chronic inflammation.

Group Members

Regis Dieckmann
Postdoctoral Fellow

Jonas Elmwall
PhD student

 

Latest publications

Neutrophil recruitment to inflamed joints can occur without cellular priming.
Lena Björkman, Karin Christenson, Lisa Davidsson, Jonas Mårtensson, Firoozeh Amirbeagi et al.
Journal of leukocyte biology, Journal article 2019
Journal article

Galectin-3 enhances monocyte-derived macrophage efferocytosis of apoptotic granulocytes in asthma
M. Erriah, K. Pabreja, M. Fricker, K. J. Baines, L. E. Donnelly et al.
Respiratory Research, Journal article 2019
Journal article

Showing 81 - 90 of 117

2002

Synaptotagmin II could confer Ca(2+) sensitivity to phagocytosis in human neutrophils.
I Maria Lindmark, Anna Karlsson, Lena Serrander, Patrice Francois, Daniel Lew et al.
Biochimica et biophysica acta, Journal article 2002
Journal article

Phagocyte activation by Trp-Lys-Tyr-Met-Val-Met, acting through FPRL1/LXA4R, is not affected by lipoxin A4.
T Christophe, Anna Karlsson, M-J Rabiet, F Boulay, Claes Dahlgren
Scandinavian journal of immunology, Journal article 2002
Journal article

The presence of stomatin in detergent-insoluble domains of neutrophil granule membranes
Elisabeth Feuk-Lagerstedt, Marie Samuelsson, Wilhelm Mosgoeller, Charlotta Movitz, Åsa Rosqvist et al.
J Leukoc Biol, Journal article 2002
Journal article

2001

Showing 81 - 90 of 117

Page Manager: Karin Allander|Last update: 9/19/2019
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