IMB Centre for Inflammation and Disease Research

Professor Matt Sweet

Associate Professor Kate Schroder

Professor Jenny Stow

Professor David Fairlie

Dr Joseph Powell


Professor Matt Sweet

Director

Email: m.sweet@imb.uq.edu.au

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Researcher ID 

Group Sweet IMB

Associate Professor Matt Sweet’s research focuses on pattern recognition receptors, macrophage biology and inflammation. Specifically, his research is aimed at understanding the molecular pathways controlling Toll-like Receptor (TLR) and Nod-like Receptor (NLR) signaling, and the functions of downstream TLR target genes in host defence and inflammation. His current research is focused on the identification, in vivo validation, and selective targeting of specific inflammatory pathways, with the goal of contributing to the development of new pharmacological agents with anti-inflammatory properties.

 

Approaches include:

  • signaling pathway analysis using cell biology and biochemical approaches
  • molecular analysis of gene regulation and function in innate immune cells
  • cell biology of primary human and mouse macrophages and epithelial cells
  • transgenic animal models for myeloid-specific gene expression and functional analysis
  • probing inflammatory signaling pathways with new chemical entities.

 

Selected inflammation publications: 

View more publications by Associate Professor Sweet via Pubmed or UQ Researchers.

Schaale K, Peters KM, Murthy AM, Fritzsche AK, Phan MD, Totsika M, et al. Strain- and host species-specific inflammasome activation, IL-1beta release, and cell death in macrophages infected with uropathogenic Escherichia coli. Mucosal Immunol. 2016;9(1):124-36.

Kapetanovic R, Bokil NJ, Achard ME, Ong CY, Peters KM, Stocks CJ, et al. Salmonella employs multiple mechanisms to subvert the TLR-inducible zinc-mediated antimicrobial response of human macrophages. Faseb j. 2016.

Ariffin JK, Kapetanovic R, Schaale K, Gatica-Andrades M, Blumenthal A, Schroder K, et al. The E3 ubiquitin ligase RNF144B is LPS-inducible in human, but not mouse, macrophages and promotes inducible IL-1beta expression. J Leukoc Biol. 2016.

Luo L, Wall AA, Yeo JC, Condon ND, Norwood SJ, Schoenwaelder S, et al. Rab8a interacts directly with PI3Kgamma to modulate TLR4-driven PI3K and mTOR signalling. Nat Commun. 2014;5:4407.

Shakespear MR, Hohenhaus DM, Kelly GM, Kamal NA, Gupta P, Labzin LI, et al. Histone deacetylase 7 promotes Toll-like receptor 4-dependent proinflammatory gene expression in macrophages. J Biol Chem. 2013;288(35):25362-74.

Schroder K, Irvine KM, Taylor MS, Bokil NJ, Le Cao KA, Masterman KA, et al. Conservation and divergence in Toll-like receptor 4-regulated gene expression in primary human versus mouse macrophages. Proc Natl Acad Sci U S A. 2012;109(16):E944-53.

Shakespear MR, Halili MA, Irvine KM, Fairlie DP, Sweet MJ. Histone deacetylases as regulators of inflammation and immunity. Trends Immunol. 2011;32(7):335-43.

 


Associate Professor Kate Schroder

Deputy Director

Email: k.schroder@imb.uq.edu.au

Group Schroder IMB

Dr Kate Schroder’s laboratory researches the molecular and cellular mechanisms by which inflammasomes and Nod-like Receptors drive inflammation during infection and disease. Her current research focuses on signal integration between inflammasomes and other innate immune pathways (e.g. Toll-like Receptors, autophagy), the biochemical mechanisms governing inflammasome and caspase activity, the evolutionary biology of Nod-like Receptors and inflammasomes, the cellular mediators of inflammasome-dependent inflammation, and the development and potential applications of novel inflammasome inhibitors.

 

Approaches include:

  • Monitoring and modulating the inflammasome pathway in human and murine myeloid cells
  • Imaging the cellular consequences of inflammasome activation
  • Interrogating the inflammasome pathway in murine models of in vivo disease
  • Molecular and cellular approaches to understanding drug mode-of-action in disease.

 

Selected inflammation publications: 

 

 

 

 

 

 

 

 

 

 


Professor Jenny Stow

Investigator

Email: j.stow@imb.uq.edu.au

Group Stow IMB

Professor Jenny Stow is a molecular cell biologist whose research is focused on understanding key trafficking pathways, membrane domains, and cell compartments in immune cells and epithelia. The Stow lab is interested in how macrophages phagocytose or eat pathogens and how macrophages secrete inflammatory cytokines – both of these cell functions contribute significantly to inflammation in immunity and in chronic disease. The team is focused on defining the role of specific druggable protein targets as a means for modulating cytokine release in chronic disease. A goal of this work is to be able to manipulate cytokines in order to switch off harmful inflammatory reactions. 

 

Approaches include:

  • Advanced fluorescence imaging in live cells, quantitative imaging and electron microscopy
  • Cell based assays for phagocytosis, secretion, endocytosis and signaling
  • Cell lines, mini-organ cultures and transgenic animal models
  • Molecular biology, gene engineering, biosensors and biochemistry to explore molecular interactions in inflammation.  

 

Selected inflammation publications: 

 

 

 

 

 

 

 

 


Professor David Fairlie

Investigator

Email: d.fairlie@imb.uq.edu.au

Group Fairlie IMB

Professor David Fairlie is internationally known in drug discovery, medicinal chemistry and pharmacology. His research in inflammation is aimed at understanding the molecular basis of immunity, disease development and drug action; intervening in the pathogenesis of inflammatory diseases; medicinal chemistry aimed at new treatments that modulate disease; and pharmacology studies aimed at interrogating molecular mechanisms of drug action in cells and in animal models.

 

Approaches include:

  • pathway- and disease-specific modulation of inflammation in vivo
  • developing agonists and antagonists of GPCRs, enzymes and inflammatory proteins
  • downsizing inflammatory proteins to small molecules
  • interrogating and modulating inflammatory signaling pathways
  • pharmacologically profiling experimental drugs in rodent models of inflammatory diseases
  • tracking and imaging labeled drugs, protein targets, immune cells and tissues.

 

Selected inflammation publications:

 

 

 

 

 

 

  • Kjer-Nielsen L, Patel O, Nours JL, Meehan B, Corbett AJ, Liu L, Bhati M, Chen Z, Kostenko L, Reantragoon R, Williamson NA, Purcell AW, Dudek NL, McConville MJ, O’Hair RAJ, Khairallah GN, Godfrey DI, Fairlie DP, Rossjohn J, McCluskey J. (2012). MR1 presents microbial vitamin metabolites to MAIT cells. Nature491, 717-723.

 

 

 

 


Dr Joseph Powell

Investigator

Email: joseph.powell@uq.edu.au

Group Powell IMB

Dr Joseph Powell uses large-scale, high-throughput genomic data to investigate how DNA sequence variants contribute to human disease. His research engages sophisticated statistical methodology and the use of high performance computing resources for novel analyses and methods development. His group is committed to both open-source and reproducible research practices.

 

Approaches include:

  • The investigation of differences in the genetic regulation of genes across tissues and cell types. We are interested in whether this can explain some of the tissue specific pathology of disease.
  • The development of novel methodology to provide flexible and efficient approaches to help determine the biological mechanisms underlying human disease. In silico methods are first used as a stepping-stone, prior to collaborating with colleagues to design molecular genomics studies to delineate the exact mechanisms.
  • The development of computational tools and apps to integrate methods and data to aid in the clinical diagnosis of disease using genomic information.

 

Selected inflammation publications:

  • Powell, J. E., Henders, A. K., McRae, A. F., Wright, M. J., Martin, N. G., Dermitzakis, E. T., Montgomery, G. W., Visscher, P. M. (2012) Genetic control of gene expression in whole blood and lymphoblastoid cell lines is largely independent. Genome Research, 22, 456-66

 

  •  The GIANT Consortium. (2014) Defining the role of common variation in the genomic and biological architecture of adult human height. Nature Genetics, 46 (11), 1173-1186.

 

  • Powell, J. E., Visscher, P. M. and Goddard, M. E. (2010) Reconciling the analysis of IBD and IBS in complex trait studies. Nature Reviews Genetics, 11, 800-805

 

  • Powell, J. E., Henders, A. K., McRae, A. F., Kim, J., Hemani G., Martin, N. G., Dermitzakis, E., Gibson, G., Montgomery, G. W., Visscher, P. M. (2013) Congruence of additive and non-additive effects on gene expression estimated from pedigree and SNP data. PLoS Genetics, 9, e1003502

 

  • Powell, J. E.*, McEvoy, B. P.*, Goddard, M. E. and Visscher, P. M. (2011) Human population dispersal “out of Africa” estimated from linkage disequilibrium and allele frequencies of SNPs. Genome Research, 21, 821-829 * Joint first

 

  • Hemani, G., Shakhbazov, K., Westra H., Esko, T., Henders, A. K., McRae, A. F., Yang, J., Gibson, G., Martin, M. G., Metspalu A., Franke, L., Montgomery, G. W., Visscher, P. M., Powell, J. E. (2014) Detection and replication of epistasis influencing transcription in humans. Nature, 508, 249-253

 

  • Gordon, L. Joo, E. J. Powell, J. E., et al. (2012) Neonatal DNA methylation profile in human twins is specified by a complex interplay between intrauterine environmental and genetic factors, subject to tissue-specific influence. Genome Research, 22, 1395-405

 

  • Yang, J., Loos, R. J. F., Powell, J. E., et al. (2012) FTO genotype is associated with phenotypic variability of body mass index. Nature, 490, 267-72

 

  • Westra, H. J., et al. (2013) Systematic identification of trans eQTLs as putative drivers of known disease associations. Nature Genetics, 45, 1238-43

 

  • Goldinger, A., Henders, A., McRae, A. F., Martin, N. G., Gibson, G., Montgomery, G. W., Visscher, P. M., Powell, J. E. (2013) Genetic and non-genetic variation revealed for the principal components of human gene expression. Genetics, 195, 1117-28

 

  • The CHARGE Consortium (Powell, J. E. Joint first) The transcriptional landscape of age in human peripheral blood. Nature Communications, In Press