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Research team

Demirel Group

About this team

Team information

The Demirel groups research interests are in the field of host-pathogen interaction and kidney disease. The increasing prevalence of antibiotic resistance emphasises the need for more in-depth knowledge about host-pathogen interaction in order to development new therapeutic strategies against bacterial infection. We need to elucidate how bacteria modulates the host immune responses in order to identify new therapeutic bacterial targets. Most of the research conducted today in the field of host-pathogen interaction is focused on elucidating how pathogens, with their respective virulence factors, successfully modulate or evade the immune responses to cause infections. However, less is known about how host immune factors like cytokines and hormones are affecting the virulence of bacteria by cross-kingdom interactions. Understanding how the human host affects the virulence of bacteria may be a new frontier in the fight against bacterial infection. It is now evident that bacterial virulence is regulated by detection of host factors released in the micro-environment like hormones and cytokines. If we can elucidate how bacteria senses its environment and mobilizes its virulence, we may inhibit this activation and dampen or completely prevent infection. By focusing of inhibiting virulence, we reduce antibiotic selection pressure, which will lead to reduced antibiotic resistance.

Key question that the group are trying to answer are:

1. How does uropathogenic E. coli virulence factors contribute to the development of urosepsis? 
2. How does renal fibroblast contribute to the host response during a urinary tract infection? 
3. How does Indoleamine 2,3-dioxygenase (IDO) and inflammasomes contribute to bacterial infections? 
4. What impact does proinflammatory cytokines and hormones have on the virulence of uropathogenic E. coli and Porphyromonas gingivalis? 
5. How does Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans contribute to oral-and systemic disease? 
6. How does the microbiota-generated metabolite TMAO contribute to the development of kidney disease?  

Funding

The Knowledge Foundation och Region Örebro län forskningskommittén

Collaborators

Katarina Persson, Örebro University
Robert Kruse, Örebro University
Ignacio Rangel, Örebro University
Ashok Kumawat, Örebro University
Geena Paramel, Örebro University
Boxi Zhang, Karolinska Institute
BEA Core facility, Karolinska Institute
Tataa Biocenter AB
Adlego Biomedical AB