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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.


Professor Anna Karlsson


Anna Karlsson

Box 480, 405 30 Göteborg

Guldhedsgatan 10 A

031-342 46 79

Sidansvarig: kommunikation@medicine.gu.se|Sidan uppdaterades: 2010-09-23

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