Reinventing the fight against bacteria,
one phage at a time.

The LEO Foundation has awarded a new translational research grant to an international consortium led by Thomas Sicheritz-Pontén at the University of Copenhagen and Martha Clokie at the Becky Mayer Centre for Phage Research, University of Leicester. The project aims to accelerate the development of bacteriophage therapy against invasive Group A Streptococcus (GAS), the bacterium responsible for necrotizing soft tissue infections (NSTIs), commonly known as "flesh-eating disease". Thomas Sicheritz-Ponten - Linkedin With this latest award, the LEO Foundation has now committed a total of 12 million DKK (approximately €1.6 million) across three complementary research projects, each funded at around 4 million DKK. Rather than supporting isolated studies, the Foundation is investing in a long-term research strategy that spans the entire innovation pipeline, from fundamental phage disco...

Bacteriophages do not infect human cells, but this does not make them immunologically invisible. The distinction between cellular tropism and immune recognition is fundamental to understanding phage therapy because the mammalian innate immune system does not determine whether a viral particle is capable of completing a productive replication cycle before responding to it. Instead, it detects molecular structures that appear in particular cellular compartments and interprets their presence as evidence of microbial invasion, cellular damage or abnormal nucleic acid localization. A bacteriophage entering a human tissue is therefore exposed to an immune surveillance system organized around molecular patterns and intracellular geography rather than around the biological category of the particle itself. DNA confined within the nucleus or mitochondria is expected, whereas DNA appearing in the cytosol can trigger innate immune signaling.  The Phage Therapy, Copyright 4.0 Nucleic acids deli...

Inflammatory bowel disease is usually described through the language of immune dysregulation, chronic inflammation and genetic susceptibility. Yet an increasingly important part of the disease may lie in a more dynamic layer of biology: not simply which microorganisms inhabit the intestine, but what particular bacterial populations are doing inside it. A new study from McMaster University pushes this idea toward a striking therapeutic possibility. Instead of broadly eliminating bacteria associated with disease, bacteriophages may be used to selectively suppress the bacterial traits that help drive inflammation. McMaster researchers, from left, Kyle Jackson, Zeinab Hosseinidoust and Elena Verdu, have found a way to disarm harmful gut bacteria using precision viruses, opening the door to more personalized treatments for inflammatory bowel disease. (Georgia Kirkos, McMaster University) The work, published in Science Translational Medicine and highlighted on the journal’s cover, emerged...

For decades, phage therapy has been described through an apparently straightforward biological relationship. A bacteriophage encounters a susceptible bacterium, recognizes a surface receptor, injects its genome, replicates and eventually destroys its host. When translated into therapeutic language, the reasoning seems almost equally simple: identify a phage capable of lysing the pathogen and administer enough viral particles to control the infection. The reality inside the human body is considerably less linear. A therapeutic bacteriophage does not move through an empty vessel containing only its bacterial host. From the moment it is administered, it encounters epithelial barriers, mucus, soluble proteins, circulating antibodies, phagocytic cells and highly organized innate and adaptive immune networks. At the same time, the bacterial population itself is changing under the combined pressure of viral predation and host immunity. Phage therapy is therefore not fundamentally a two-player...