Innate immune cells, such as macrophages, express a broad repertoire of pattern recognition receptors that act as danger sensors. For example, members of the Toll-like receptor (TLR) family detect a number of pathogen-associated molecular patterns such as LPS from Gram-negative bacteria. Macrophage activation through TLRs regulates expression of genes involved in antimicrobial responses and inflammation. Thus, TLR signalling is required for effective control of invading microorganisms, but if dysregulated, contributes to acute and chronic inflammatory diseases.

Our team studies TLR signalling pathways and the functions of TLR-regulated genes in inflammation and in responses to bacterial pathogens (e.g. Salmonella, uropathogenic E. coli).

Traineeships, honours and PhD projects include

  • TLR-inducible zinc toxicity as a macrophage antimicrobial weapon against bacterial pathogens
  • Reprogramming of macrophage functions as anti-infective strategy against bacterial pathogens such as Salmonella and uropathogenic E. coli
  • Characterization and targeting of TLR-inducible pro-inflammatory signalling in macrophages
  • Roles of protein deacetylases in innate immunity
  • Regulated immunometabolism in macrophages

Project members

Group Leader

Professor Matt Sweet

Director, IMB Centre for Inflammation & Disease Research
Professorial Research Fellow
Institute for Molecular Bioscience