
Magnus Höök
Professor of IBT-Houston
molecular microbial pathogenesis, protein interactions, protein engineering, vaccine and antibiotics discovery, translational research and entrepreneurship
Our goal is to understand in molecular terms how microbes cause disease. We see this process
as a molecular war between the attacking microbe and the defending host (humans). The
molecular weapons of the microbe will typically interact with and manipulate different defense
systems in the host. As we uncover the weak points in the microbe’s attack, we seek to target
these by developing novel therapeutics and vaccines. Promising new drugs are tested in
different models and ultimately in the clinic. This process involves close interactions with
pharma and biotech companies.
Staphylococcus aureus and the Fibrinogen shield
Staphylococcus aureus is an opportunistic pathogen which colonize the surfaces of our body
without causing disease. However, if the microbe can get access to the interior of the host it
can cause life threatening infections such as endocarditis, pneumonia, sepsis and osteomyelitis. A common feature of these infections is that the bacteria is spread through the blood where
they face a hostile environment. To survive the microbe protect itself from the antimicrobial
agents in blood S. aureus by assembling a fibrinogen shield around the bacteria. We are using a
biochemical approach to determine the molecules and processes involved in the formation of
this shield.
Why do some Staphylococcus epidermidis strains cause serious infections?
S. epidermidis has for decades been regarded as a harmless colonizer of our skin. With the
increasing use of foreign body implants, some strains of S. epidermidis have found a niche where they are uniquely suited to colonize the surface of this implant. In this process, they come in contact with body fluids including blood. Recent work has shown that a few strains of S. epidermidis now can cause serious bloodstream infections. We will determine what
molecules in the infective isolates are responsible for causing disease. In these studies, we
collaborate with clinicians and use a combination of genetic and biochemical approaches.
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