Miguel Soares

Miguel Che Parreira Soares
Fundação Calouste Gulbenkian, Oeiras
Project Leader

Metabolic reprograming in sepsis.

• Michael Bauer
  Friedrich-Schiller- Universität Jena (FSU), Jena

Sepsis is a life-threatening disease where an uncontrolled response to infection leads to multi organ failure. Antibiotics alone are not sufficient to treat sepsis, which kills over 11 million individuals per year worldwide. As such we propose to develop a therapeutic approach that instead of killing bacteria prevents the development of organ dysfunction and enhances the capacity to endure the infection. The rational for this approach is based on our previous finding that mice and humans share a genetic program, activated in response to bacterial infection and preventing the development of organ failure, without killing the bacteria. We propose to:

1. Identify genes regulated by this genetic program.

2. Determine their protective effect in experimental models of sepsis in mice.

3. Correlate their expression with the outcome of clinical sepsis in humans, towards the discovery of new therapeutic targets and strategies to reduce the global burden of sepsis.

Miguel Soares is the Group Leader of the Inflammation Laboratory at the Instituto Gulbenkian de Ciência. He has also been an Invited professor at Lisbon Medical Schools of Universidade de Lisboa for almost 20 years and of the newly established Universidade Católica de Lisboa, for the last 3 years. Soares graduated BS in biology, he did a MS in cellular biology and a Ph.D. in Science from the University of Louvain in Belgium. He did his research fellowship with Prof. Fritz H. Bach. He then was instructor in surgery and lecturer at the Beth Israel Deaconess Medical Center, at the Harvard Medical School (USA). (Read full CV).

Immunity volved in multicellular organisms to limit the fitness costs imposed by interactions with microbes, a defense strategy referred to as resistance to infection. In addition, there is another evolutionary conserved defense strategy that does not exert a direct negative impact on microorganisms, referred as disease tolerance. This defense strategy acts, at an organismal level, to limit metabolic dysfunction and tissue damage, imposed by pathogenic microorganisms or by immune-driven resistance mechanisms. The objective of our research efforts is to identify and characterize how stress and damage responses provide metabolic adaptation to establish disease tolerance to viral, bacterial or protozoan infections.

Miguel Soares, PhD
Principal Investigator / Inflammation

Tel.: (+351) 214 464 520

Instituto Gulbenkian de Ciência
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