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Fredrik KahnBacterial manipulation of host defence systems in sepsis

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Department of Clinical Sciences, Infection Medicine, Lund University

My work focuses on bacterial-host interactions and manipulation of these in sepsis. As model pathogens I have chosen Streptococcus pyogenes (Group A Streptococcus) and Streptococcus agalactiae (Group B Streptococcus).

My previous studies have shown that S. pyogenes can use antibodies to over activate the immune system and thereby induce a vascular leakage. A massive vascular leakage is a hallmark of severe infections with S. pyogenes. Severe sepsis is often accompanied by thrombocytopenia. Much less is known why thrombocytopenia develops.

Recently, platelets have been recognised for their possible role in host defence. However, we have, in a model, shown that induced thrombocytopenia reduces the dissemination of infection. We plan to further characterize the platelet-pathogen interaction and its consequences for the host. Can this interaction be manipulated and does this alter the progression of the disease? S. agalactiae is the most common pathogen in neonatal life-threatening bacterial infections but has also an increasing incidence among elderly.

It often gives rise to pneumonia, sepsis and meningitis. sPLA2-IIA (group IIA secreted phospholipase A2) is one of the members in the family of phospholipases A2. These enzymes digest phospholipids into lysophospholipids and free fatty acids. Previous studies have indicated that sPLA2-IIA is a part of innate immunity and especially effective against Gram-positive pathogens. S. agalactiae has proven to be extremely sensitive to sPLA2-IIA. In our studies we focus on the host response of sPLA2-IIA to investigate if this enzyme takes part and modulates the course of S. agalactiae infections.



footer all slides 2014-02-06


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