Staffan Normark has been a professor in Medical Microbiology at MTC since 1993. Before that he had similar positions in Umea and in Saint Louis.
The main research interest is host-bacterial interactions. This spans many projects, ranging from bacterial regulatory systems to the immune response of the host. Much work is done together with other groups in a larger constellation of researchers to facilitate introduction of new techniques and ideas.
Our research focuses mainly on host-bacterial interactions, with projects ranging from bacterial regulatory systems to innate immune responses in the host. the main research program includes studies on the molecular epidemiology and pathogenesis of pneumococcal infections, from the clinical side to more basic approaches looking at host-pathogen interactions. Also, antibiotic resistance development is targeted.
Streptococcus pneumoniae is a common cause of morbidity and mortality worldwide, killing 1–2 million people every year. Despite being a devastating pathogen they are also frequent colonizers of the upper respiratory tract of healthy children attending day-care centers. We have studied the molecular epidemiology of invasive pneumococcal disease and found that certain serotypes and clones are more prone to give raise to invasive disease, such as clones of type 1 and 7F. These types are more commonly found among previously healthy individuals. We have also identified novel virulence factors such as a pilus like structure important for adherence, colonization, and virulence, as well as for the inflammatory response. Furthermore we have shown that pneumococci are trapped but not killed by so called neutrophil extracellular traps (NETs). However, the bacteria may free themselves from NETs by using an endonuclease, thereby promoting spread to the lungs and the bloodstream. Recently we have found that of the Toll-like receptors (TLR) 1,2,4,6 and 9, only TLR 9 plays a non-redundant role in pneumococcal infections. Other research includes studies of inhibitors of the type III secretion system in Chlamydia trachomatis, an enzymatic ruler that modulates Lewis antigen glycosylation of Helicobacter pylori lipopolysaccharide during persistent infection, antimicrobial peptides, and invasive Group a streptococcal infections. We will also continue our work on the recently describe pilus-like structure and other potential vaccine candidates, as well as on type III secretion inhibitors for drug development.
The work can tentatively be divided into the following areas:
1.
The innate immune defense and bacterial infections.
The interaction between the innate immune system and microbial pathogens including for example Toll like receptors, NODs, scavenger receptors and antimicrobial peptides.
2.
Streptococcus pneumoniae (pneumococci).
Involves many aspects of this pathogen, ranging from its epidemiology and antibiotic resistance to virulence and pathogenesis aspects and the interaction with the innate immune system.
3.
Helicobacter.
To understand the interactions with the host and why some strains are more virulent than others.
4.
Regulation of virulence genes.
Escherichia coli and Salmonella are the main models to look at gene regulatory mechanisms involved in virulence and adaptation to new environments.
5.
Bacterial adhesion organelles.
Studying the biogenesis of adhesion organelles, such as pili and curli. But also their role in disease.
6.
Cell wall synthesis.
Includes projects from reageneration of cell wall components and programmed cell death in bacteria to the function and regulation of beta-lactamases.
7.
Chlamydia species.
Specifically we are studying inhibitors of the type III secretion system.
Department of Microbiology, Tumor and Cell Biology (MTC)
Karolinska Institutet
Box 280
SE-171 77
Stockholm
Sweden
Phone: +46-8-4572418
E-mail:
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