Professor Matt Sweet

NHMRC Leadership Fellow - GL

Institute for Molecular Bioscience

Affiliated Professor

School of Chemistry and Molecular Biosciences
Faculty of Science
m.sweet@imb.uq.edu.au
+61 7 334 62082

Overview

Matt Sweet is an NHMRC Leadership Fellow and Group Leader at the Institute for Molecular Bioscience (IMB) at The University of Queensland, Brisbane, Australia. He was the founding Director of the IMB Centre for Inflammation and Disease Research (2014-2018), and also served as Deputy Head of the IMB Division of Cell Biology and Molecular Medicine during this period. Matt studies innate immunity, the body’s danger sensing system that responds to infection, injury and dysregulated homeostasis, and the role of this system in health and disease. Matt’s research team is focused on characterizing the roles of specific innate immune pattern recognition receptors and their downstream signalling pathways/gene products in inflammatory disease processes, as well as in host responses to bacterial pathogens. He has authored >150 journal articles and book chapters, including in Science (2), Science Translational Medicine, Science Immunology, Nature Genetics, Nature Communications(2),PNAS USA (3) and Journal of Experimental Medicine (2), and his career publications have accrued ~13,500 citations.

Biography

I was awarded a PhD (The University of Queensland) in 1996 for my research under the supervision of Prof David Hume into gene regulation in macrophages, immune cells with important roles in health and disease. I subsequently undertook a short postdoctoral position in the same laboratory, focusing on the activation of macrophages by pathogen products. I then embarked on a CJ Martin post-doctoral training fellowship with Prof Eddy Liew, FRS at the University of Glasgow in Scotland. Returning to The University of Queensland, I had a prominent role within the Cooperative Research Centre for Chronic Inflammatory Diseases (including as UQ node head from 2007-2008) and was appointed as a Group Leader at the IMB in 2007. I have continued fellowship support since this time, including as an ARC Future Fellow, an NHMRC Senior Research Fellow and an NHMRC Leadership Fellow (current, from 2021).

Key discoveries

CpG-containing DNA as an activator of innate immunity, and characterization of the receptor (TLR9) detecting this microbial component.

The IL-1 receptor family member ST2 as a critical regulator of innate immunity and inflammation.

Inflammatory and antimicrobial functions of histone deacetylase enzymes (HDACs) in macrophages.

Effects of the growth factor CSF-1 on inflammatory responses in macrophages.

Mechanisms responsible for divergence in TLR responses between human and mouse macrophages, as well as the functional consequences of such divergence.

TLR-inducible zinc toxicity as an antimicrobial weapon of macrophages.

Host evasion strategies used by the bacterial pathogens Salmonella enterica serovar Typhimurium and uropathogenic E. coli.

SCIMP as a novel TLR adaptor that mediates TLR tyrosine phosphorylation and selective cytokine outputs.

Genes and pathways associated with the severity of chronic liver disease.

Molecular mechanisms controlling macrophage immunometabolism, as well as associated inflammatory and antimicrobial responses.

Research training

I have supervised or co-supervised 24 completed PhD students and 21 completed honours students, as well as 9 post-doctoral researchers. Many of my former staff and students continue to have active research careers around the world (USA, UK, Europe, Australia), including as independent laboratory heads. I currently supervise 5 PhD students in my laboratory, co-supervise 5 PhD students in other laboratories, and oversee the research activities of 2 post-doctoral researchers in my group. Current and former staff/students have received numerous fellowships and awards during their research careers (e.g. ARC DECRA, NHMRC CJ Martin fellowship, UQ post-doctoral fellowship, Smart State scholarship). I have also examined 22 PhD theses in the fields of innate immunity, inflammation and host defence.

Professional activities

I am an editorial board member of the Journal of Leukocyte Biology, Immunology and Cell Biology, Seminars in Cell & Developmental Biology, and Frontiers in Immunology. I have served on NHMRC project grant review panels in 2007, 2008, 2009, 2012 (as panel chair) and 2014, as well as a member of the NHMRC RGMS user reference group committee from 2010-2012. I acted as national representative for the Australasian Society of Immunology (ASI) Infection and Immunity special interest group from 2012-2017. At UQ, I served as chair of an animal ethics committee from 2013-2014, and co-organized the UQ Host-Pathogen interaction network from 2007-2010 (prior to the establishment of the Australian Infectious Diseases Research Centre).

I have made extensive contributions to conference organization in my discipline. I co-organized the national TLROZ2009 and TLROZ2012 conferences, I organized the first ever Australasian Society for Immunology (ASI) Infection and Immunity workshop (2009), was chair of the ASI Program Committee and co-organizer of the Infection and Immunity workshop for ASI2017, and I co-organized the annual IMB Inflammation Symposium (2014-2018). I also co-chaired the 2019 World Conference of Inflammation (Sydney, September 2019). In addition, I have been a member of the organizing committee for ASI2009, the 2014 International Cytokine and Interferon Society conference, the Lorne Infection and Immunity conference (2014-2020), and the Brisbane Immunology Group annual meeting (2008 to the present).

Research Interests

  • INNATE IMMUNE INFLAMMATORY PATHWAYS
    Cells of the innate immune system such as macrophages play essential roles in detecting and responding to danger, which can be sensed as a result of infection, injury and/or dysregulated homeostasis. These cells use several families of pattern recognition receptors (PRRs), such as the toll-like receptors (TLRs) and nod-like receptors (NLRs), to recognize specific danger signals. Inappropriate or prolonged PRR activation drives dysregulated inflammation, which is central to the pathology of many acute and chronic diseases. Current research is focused on developing approaches to target PRR signaling pathways and other innate immune pathways for potential applications in inflammatory diseases such as chronic liver disease, sepsis and inflammatory bowel diseases. Areas of specific interest including (1) characterizing mechanisms by which novel TLR complex components provide specificity to inflammatory responses; (2) control of inflammatory outputs by immune cell metabolism and (3) the roles of individual histone deacetylase enzymes, particularly HDAC7, in macrophage inflammatory pathways and inflammatory disease processes.
  • INNATE IMMUNE ANTIMICROBIAL PATHWAYS
    Innate immunity plays a pivotal role in protecting against invading microorganisms. Successful pathogens must overcome this system to colonize the host and cause disease. Many important pathogens actively target macrophages, residing in these cells or destroying them to avoid immune defence. We study TLR-inducible macrophage antimicrobial responses, and how the Gram-negative bacterial pathogens Salmonella enterica serovar Typhimurium (S. Typhimurium) and uropathogenic E. coli (UPEC) are able to overcome such responses. Our focus is on developing novel anti-infective strategies, through the manipulation of innate immune antimicrobial responses. Areas of specific interest include (1) characterizing TLR-inducible antimicrobial responses (zinc poisoning, mitochondrial fission) in macrophages, as well as host subversion strategies; (2) defining mechanisms by which specific HDAC enzymes (HDAC6, HDAC7) regulate macrophage host defence pathways; and (3) unravelling the contributions of UPEC-triggered macrophage cell death to immune defence versus host subversion.
  • SPECIES DIFFERENCES IN INNATE IMMUNITY
    Whilst conservation of a gene or pathway across species is an obvious indicator of its importance, the fact that a gene or a pathway is not conserved does not mean that it isn’t important for one particular species. In fact, in the context of co-evolution of host and pathogen, species-specific responses are likely to be critical for host defence. We have characterized differences in TLR responses between human and mouse, and the mechanisms responsible. Our current focus is on characterizing the roles of individual TLR target genes that are differentially regulated between human and mouse in host defence against bacterial pathogens and in inflammatory responses.

Research Impacts

Every organism and every cell employs some form of innate defence for protection against agents with the ability to cause harm. In complex multicellular organisms, these innate defence systems also have the capacity to cause damage to the organism itself. As such, innate immunity lies at the heart of almost all disease processes. Our fundamental research in this field has the potential to lead to new anti-infective and/or anti-inflammatory agents that may have applications in the health, livestock and/or veterinary sectors.

Specific indicators of impact

· More than 150 career publications, which have collectively accrued ~13,500 citations (average cites/article: ~90; most cited article: >900 citations; >200 citations of my research in Cell, Science, Nature and Nature specialty journals (e.g. Nature Immunologyetc)). My publications include 35 invited review articles, editorials and book chapters, and of these, 4 reviews have received more than 200 citations, another 6 have received more than 100 citations, and 1 received the Dolph Adams award from the Journal of Leukocyte Biology. I have also been invited to guest edit review series for Seminars in Cell and Developmental Biology, Immunology and Cell Biology and Journal of Leukocyte Biology.

· Contribution to the development and/or validation of several novel small molecule inhibitors of inflammation-relevant proteins, and numerous interactions with the Pharmaceutical/Biotechnology industry.

· Identification of a gene signature associated with severity of chronic liver disease, with these findings currently being pursued for discovery of biomarkers and therapeutic targets.

· >100 invitations to speak nationally and internationally at conferences, institute/departmental seminars, and other forums. I have also chaired >30 sessions at national and international conferences.

Qualifications

  • PhD, The University of Queensland
  • BSc(Hons), The University of Queensland

Publications

  • Bosch, Marta, Sánchez-Álvarez, Miguel, Fajardo, Alba, Kapetanovic, Ronan, Steiner, Bernhard, Dutra, Filipe, Moreira, Luciana, López, Juan Antonio, Campo, Rocío, Marí, Montserrat, Morales-Paytuví, Frederic, Tort, Olivia, Gubern, Albert, Templin, Rachel M., Curson, James E. B., Martel, Nick, Català, Cristina, Lozano, Francisco, Tebar, Francesc, Enrich, Carlos, Vázquez, Jesús, Del Pozo, Miguel A., Sweet, Matthew J., Bozza, Patricia T., Gross, Steven P., Parton, Robert G. and Pol, Albert (2020). Mammalian lipid droplets are innate immune hubs integrating cell metabolism and host defense. Science, 370 (6514) 8085, 309-+. doi: 10.1126/science.aay8085

  • Stocks, Claudia J., Pein, Jessica B., Curson, James E.B., Rae, James, Phan, Minh‐Duy, Foo, Darren, Bokil, Nilesh J., Kambe, Taiho, Peters, Kate M., Parton, Robert G., Schembri, Mark A., Kapetanovic, Ronan and Sweet, Matthew J. (2020). Frontline Science: LPS‐inducible SLC30A1 drives human macrophage‐mediated zinc toxicity against intracellular Escherichia coli. Journal of Leukocyte Biology, 109 (2) JLB.2HI0420-160R, 287-297. doi: 10.1002/jlb.2hi0420-160r

  • Das Gupta, Kaustav, Shakespear, Melanie R., Curson, James E.B., Murthy, Ambika M.V., Iyer, Abishek, Hodson, Mark P., Ramnath, Divya, Tillu, Vikas A., von Pein, Jessica B., Reid, Robert C., Tunny, Kathryn, Hohenhaus, Daniel M., Moradi, Shayli Varasteh, Kelly, Gregory M., Kobayashi, Takumi, Gunter, Jennifer H., Stevenson, Alexander J., Xu, Weijun, Luo, Lin, Jones, Alun, Johnston, Wayne A., Blumenthal, Antje, Alexandrov, Kirill, Collins, Brett M., Stow, Jennifer L., Fairlie, David P. and Sweet, Matthew J. (2020). Class IIa histone deacetylases drive toll-like receptor-inducible glycolysis and macrophage inflammatory responses via pyruvate kinase M2. Cell Reports, 30 (8), 2712-2728.e8. doi: 10.1016/j.celrep.2020.02.007

  • Yang, Yoon Mee, Noureddin, Mazen, Liu, Cheng, Ohashi, Koichiro, Kim, So Yeon, Ramnath, Divya, Powell, Elizabeth E., Sweet, Matthew J., Roh, Yoon Seok, Hsin, I-Fang, Deng, Nan, Liu, Zhenqiu, Liang, Jiurong, Mena, Edward, Shouhed, Daniel, Schwabe, Robert F., Jiang, Dianhua, Lu, Shelly C., Noble, Paul W. and Seki, Ekihiro (2019). Hyaluronan synthase 2–mediated hyaluronan production mediates Notch1 activation and liver fibrosis. Science Translational Medicine, 11 (496) eaat9284, eaat9284. doi: 10.1126/scitranslmed.aat9284

  • Stocks, Claudia J., Phan, Minh-Duy, Achard, Maud E. S., Nhu, Nguyen Thi Khanh, Condon, Nicholas D., Gawthorne, Jayde A., Lo, Alvin W., Peters, Kate M., McEwan, Alastair G., Kapetanovic, Ronan, Schembri, Mark A. and Sweet, Matthew J. (2019). Uropathogenic Escherichia coli employs both evasion and resistance to subvert innate immune-mediated zinc toxicity for dissemination. Proceedings of the National Academy of Sciences, 116 (13), 6341-6350. doi: 10.1073/pnas.1820870116

  • Ramnath, Divya, Irvine, Katharine M., Lukowski, Samuel W., Horsfall, Leigh U., Loh, Zhixuan, Clouston, Andrew D., Patel, Preya J., Fagan, Kevin J., Iyer, Abishek, Lampe, Guy, Stow, Jennifer L., Schroder, Kate, Fairlie, David P., Powell, Joseph E., Powell, Elizabeth E. and Sweet, Matthew J. (2018). Hepatic expression profiling identifies steatosis-independent and steatosis-driven advanced fibrosis genes. JCI Insight, 3 (14). doi: 10.1172/jci.insight.120274

  • Shakespear, Melanie R., Iyer, Abishek, Cheng, Catherine Youting, Das Gupta, Kaustav, Singhal, Amit, Fairlie, David P. and Sweet, Matthew J. (2018). Lysine deacetylases and regulated glycolysis in macrophages. Trends in Immunology, 39 (6), 473-488. doi: 10.1016/j.it.2018.02.009

  • Luo, Lin, Bokil, Nilesh J., Wall, Adam A., Kapetanovic, Ronan, Lansdaal, Natalie M., Marceline, Faustine, Burgess, Belinda J., Tong, Samuel J., Guo, Zhong, Alexandrov, Kirill, Ross, Ian L., Hibbs, Margaret L., Stow, Jennifer L. and Sweet, Matthew J. (2017). SCIMP is a transmembrane non-TIR TLR adaptor that promotes proinflammatory cytokine production from macrophages. Nature Communications, 8 (1) 14133, 14133. doi: 10.1038/ncomms14133

  • Kapetanovic, Ronan, Bokil, Nilesh J., Achard, Maud E. S., Ong, Cheryl-lynn Y, Peters, Kate M., Stocks, Claudia J., Phan, Minh-Duy, Monteleone, Mercedes, Schroder, Kate, Irvine, Katharine M., Saunders, Bernadette M., Walker, Mark J., Stacey, Katryn J., McEwan, Alastair G., Schembri, Mark A. and Sweet, Matthew J. (2016). Salmonella employs multiple mechanisms to subvert the TLR-inducible zinc-mediated antimicrobial response of human macrophages. The FASEB Journal, 30 (5), 1901-1912. doi: 10.1096/fj.201500061

  • Schaale, K., Peters, K. M., Murthy, A. M., Fritzsche, A. K., Phan, M.-D., Totsika, M., Robertson, A. A. B., Nichols, K. B., Cooper, M. A., Stacey, K. J., Ulett, G. C., Schroder, K., Schembri, M. A. and Sweet, M. J. (2016). Strain- and host species-specific inflammasome activation, IL-1β release, and cell death in macrophages infected with uropathogenic Escherichia coli.. Mucosal Immunology, 9 (1), 124-136. doi: 10.1038/mi.2015.44

  • Luo, Lin, Wall, Adam A., Yeo, Jeremy C., Condon, Nicholas D., Norwood, Suzanne J., Schoenwaelder, Simone, Chen, Kaiwen W., Jackson, Shaun, Jenkins, Brendan J., Hartland, Elizabeth L., Schroder, Kate, Collins, Brett M., Sweet, Matthew J. and Stow, Jennifer L. (2014). Rab8a interacts directly with PI3Kγ to modulate TLR4-driven PI3K and mTOR signalling. Nature Communications, 5 (1) 4407, 4407.1-4407.13. doi: 10.1038/ncomms5407

  • Shakespear, Melanie R., Hohenhaus, Daniel M., Kelly, Greg M., Kamal, Nabilah A., Gupta, Praveer, Labzin, Larisa I., Schroder, Kate, Garceau, Valerie, Barbero, Sheila, Iyer, Abishek, Hume, David A., Reid, Robert C., Irvine, Katharine M., Fairlie, David P. and Sweet, Matthew J. (2013). Histone deacetylase 7 promotes Toll-like Receptor 4-dependent pro-inflammatory gene expression in macrophages. Journal of Biological Chemistry, 288 (35), 25362-25374. doi: 10.1074/jbc.M113.496281

  • Schroder, Kate, Irvine, Katharine M., Taylor, Martin S., Bokil, Nilesh J., Le Cao, Kim-Anh, Masterman, Kelly-Anne, Labzin, Larisa I., Semple, Colin A., Kapetanovic, Ronan, Fairbairn, Lynsey, Akalin, Altuna, Faulkner, Geoffrey J., Baillie, John Kenneth, Gongora, Milena, Daub, Carsten O., Kawaji, Hideya, McLachlan, Geoffrey J., Goldman, Nick, Grimmond, Sean M., Carninci, Piero, Suzuki, Harukazu, Hayashizaki, Yoshihide, Lenhard, Boris, Hume, David A. and Sweet, Matthew J. (2012). Conservation and divergence in Toll-like receptor 4-regulated gene expression in primary human versus mouse macrophages. Proceedings of the National Academy of Sciences of the USA, 109 (16), E944-E953. doi: 10.1073/pnas.1110156109

  • Roberts, Tara L., Idris, Adi, Dunn, Jasmyn A., Kelly, Greg M., Burnton, Carol M., Hodgson, Samantha, Hardy, Lani. L., Garceau, Valerie, Sweet, Matthew J., Ross, Ian L., Hume, David A. and Stacey, Katryn J. (2009). HIN-200 proteins regulate caspase activation in response to foreign cytoplasmic DNA. Science, 323 (5917), 1057-1060. doi: 10.1126/science.1169841

  • Sweet, Matthew J., Campbell, Carol C., Sester, David P., Xu, Damo, McDonald, Rebecca C., Stacey, Katryn J., Hume, David A. and Liew, Foo Y. (2002). Colony-stimulating factor-1 suppresses responses to CpG DNA and expression of toll-like receptor 9 but enhances responses to lipopolysaccharide in murine macrophages. Journal of Immunology, 168 (1), 392-399. doi: 10.4049/jimmunol.168.1.392

  • Sweet, M. J., Leung, B. P., Kang, D. W., Sogaard, M., Schulz, K., Trajkovic, V., Campbell, C. C., Xu, D. M. and Liew, F. Y. (2001). A novel pathway regulating lipopolysaccharide-induced shock by ST2/T1 via inhibition of toll-like receptor 4 expression. Journal of Immunology, 166 (11), 6633-6639. doi: 10.4049/jimmunol.166.11.6633

  • Stacey, K. J., Sweet, M. J. and Hume, D. A. (1996). Macrophages ingest and are activated by bacterial DNA. Journal of Immunology, 157 (5), 2116-2122.

View all Publications

Supervision

  • Doctor Philosophy

  • Doctor Philosophy

  • Doctor Philosophy

View all Supervision

Available Projects

  • We have found that specific HDAC enzymes constrain macrophage antimicrobial responses, particularly TLR-inducible mitochondrial fission. This project will explore the specific molecular mechanisms by which HDACs constrain macrophage antimicrobial pathways and will investigate novel anti-infective approaches that target HDAC enzymes.

  • Projects are available to investigate different aspects of TLR-inducible inflammatory pathways in macrophages, for example the role of a novel TLR adaptor in macrophage inflammatory responses and HDAC-mediated control of metabolic pathways in macrophage-mediated inflammation.

  • Innate immune cells deliver toxic levels of zinc to invading microorganisms as an antimicrobial strategy, with zinc-sensitive mutants of a number of pathogens compromised for defence against innate immune cells. This project will focus on the cellular and molecular mechanisms involved in initiation of this host defence pathway.

View all Available Projects

Publications

Featured Publications

  • Bosch, Marta, Sánchez-Álvarez, Miguel, Fajardo, Alba, Kapetanovic, Ronan, Steiner, Bernhard, Dutra, Filipe, Moreira, Luciana, López, Juan Antonio, Campo, Rocío, Marí, Montserrat, Morales-Paytuví, Frederic, Tort, Olivia, Gubern, Albert, Templin, Rachel M., Curson, James E. B., Martel, Nick, Català, Cristina, Lozano, Francisco, Tebar, Francesc, Enrich, Carlos, Vázquez, Jesús, Del Pozo, Miguel A., Sweet, Matthew J., Bozza, Patricia T., Gross, Steven P., Parton, Robert G. and Pol, Albert (2020). Mammalian lipid droplets are innate immune hubs integrating cell metabolism and host defense. Science, 370 (6514) 8085, 309-+. doi: 10.1126/science.aay8085

  • Stocks, Claudia J., Pein, Jessica B., Curson, James E.B., Rae, James, Phan, Minh‐Duy, Foo, Darren, Bokil, Nilesh J., Kambe, Taiho, Peters, Kate M., Parton, Robert G., Schembri, Mark A., Kapetanovic, Ronan and Sweet, Matthew J. (2020). Frontline Science: LPS‐inducible SLC30A1 drives human macrophage‐mediated zinc toxicity against intracellular Escherichia coli. Journal of Leukocyte Biology, 109 (2) JLB.2HI0420-160R, 287-297. doi: 10.1002/jlb.2hi0420-160r

  • Das Gupta, Kaustav, Shakespear, Melanie R., Curson, James E.B., Murthy, Ambika M.V., Iyer, Abishek, Hodson, Mark P., Ramnath, Divya, Tillu, Vikas A., von Pein, Jessica B., Reid, Robert C., Tunny, Kathryn, Hohenhaus, Daniel M., Moradi, Shayli Varasteh, Kelly, Gregory M., Kobayashi, Takumi, Gunter, Jennifer H., Stevenson, Alexander J., Xu, Weijun, Luo, Lin, Jones, Alun, Johnston, Wayne A., Blumenthal, Antje, Alexandrov, Kirill, Collins, Brett M., Stow, Jennifer L., Fairlie, David P. and Sweet, Matthew J. (2020). Class IIa histone deacetylases drive toll-like receptor-inducible glycolysis and macrophage inflammatory responses via pyruvate kinase M2. Cell Reports, 30 (8), 2712-2728.e8. doi: 10.1016/j.celrep.2020.02.007

  • Yang, Yoon Mee, Noureddin, Mazen, Liu, Cheng, Ohashi, Koichiro, Kim, So Yeon, Ramnath, Divya, Powell, Elizabeth E., Sweet, Matthew J., Roh, Yoon Seok, Hsin, I-Fang, Deng, Nan, Liu, Zhenqiu, Liang, Jiurong, Mena, Edward, Shouhed, Daniel, Schwabe, Robert F., Jiang, Dianhua, Lu, Shelly C., Noble, Paul W. and Seki, Ekihiro (2019). Hyaluronan synthase 2–mediated hyaluronan production mediates Notch1 activation and liver fibrosis. Science Translational Medicine, 11 (496) eaat9284, eaat9284. doi: 10.1126/scitranslmed.aat9284

  • Stocks, Claudia J., Phan, Minh-Duy, Achard, Maud E. S., Nhu, Nguyen Thi Khanh, Condon, Nicholas D., Gawthorne, Jayde A., Lo, Alvin W., Peters, Kate M., McEwan, Alastair G., Kapetanovic, Ronan, Schembri, Mark A. and Sweet, Matthew J. (2019). Uropathogenic Escherichia coli employs both evasion and resistance to subvert innate immune-mediated zinc toxicity for dissemination. Proceedings of the National Academy of Sciences, 116 (13), 6341-6350. doi: 10.1073/pnas.1820870116

  • Ramnath, Divya, Irvine, Katharine M., Lukowski, Samuel W., Horsfall, Leigh U., Loh, Zhixuan, Clouston, Andrew D., Patel, Preya J., Fagan, Kevin J., Iyer, Abishek, Lampe, Guy, Stow, Jennifer L., Schroder, Kate, Fairlie, David P., Powell, Joseph E., Powell, Elizabeth E. and Sweet, Matthew J. (2018). Hepatic expression profiling identifies steatosis-independent and steatosis-driven advanced fibrosis genes. JCI Insight, 3 (14). doi: 10.1172/jci.insight.120274

  • Shakespear, Melanie R., Iyer, Abishek, Cheng, Catherine Youting, Das Gupta, Kaustav, Singhal, Amit, Fairlie, David P. and Sweet, Matthew J. (2018). Lysine deacetylases and regulated glycolysis in macrophages. Trends in Immunology, 39 (6), 473-488. doi: 10.1016/j.it.2018.02.009

  • Luo, Lin, Bokil, Nilesh J., Wall, Adam A., Kapetanovic, Ronan, Lansdaal, Natalie M., Marceline, Faustine, Burgess, Belinda J., Tong, Samuel J., Guo, Zhong, Alexandrov, Kirill, Ross, Ian L., Hibbs, Margaret L., Stow, Jennifer L. and Sweet, Matthew J. (2017). SCIMP is a transmembrane non-TIR TLR adaptor that promotes proinflammatory cytokine production from macrophages. Nature Communications, 8 (1) 14133, 14133. doi: 10.1038/ncomms14133

  • Kapetanovic, Ronan, Bokil, Nilesh J., Achard, Maud E. S., Ong, Cheryl-lynn Y, Peters, Kate M., Stocks, Claudia J., Phan, Minh-Duy, Monteleone, Mercedes, Schroder, Kate, Irvine, Katharine M., Saunders, Bernadette M., Walker, Mark J., Stacey, Katryn J., McEwan, Alastair G., Schembri, Mark A. and Sweet, Matthew J. (2016). Salmonella employs multiple mechanisms to subvert the TLR-inducible zinc-mediated antimicrobial response of human macrophages. The FASEB Journal, 30 (5), 1901-1912. doi: 10.1096/fj.201500061

  • Schaale, K., Peters, K. M., Murthy, A. M., Fritzsche, A. K., Phan, M.-D., Totsika, M., Robertson, A. A. B., Nichols, K. B., Cooper, M. A., Stacey, K. J., Ulett, G. C., Schroder, K., Schembri, M. A. and Sweet, M. J. (2016). Strain- and host species-specific inflammasome activation, IL-1β release, and cell death in macrophages infected with uropathogenic Escherichia coli.. Mucosal Immunology, 9 (1), 124-136. doi: 10.1038/mi.2015.44

  • Luo, Lin, Wall, Adam A., Yeo, Jeremy C., Condon, Nicholas D., Norwood, Suzanne J., Schoenwaelder, Simone, Chen, Kaiwen W., Jackson, Shaun, Jenkins, Brendan J., Hartland, Elizabeth L., Schroder, Kate, Collins, Brett M., Sweet, Matthew J. and Stow, Jennifer L. (2014). Rab8a interacts directly with PI3Kγ to modulate TLR4-driven PI3K and mTOR signalling. Nature Communications, 5 (1) 4407, 4407.1-4407.13. doi: 10.1038/ncomms5407

  • Shakespear, Melanie R., Hohenhaus, Daniel M., Kelly, Greg M., Kamal, Nabilah A., Gupta, Praveer, Labzin, Larisa I., Schroder, Kate, Garceau, Valerie, Barbero, Sheila, Iyer, Abishek, Hume, David A., Reid, Robert C., Irvine, Katharine M., Fairlie, David P. and Sweet, Matthew J. (2013). Histone deacetylase 7 promotes Toll-like Receptor 4-dependent pro-inflammatory gene expression in macrophages. Journal of Biological Chemistry, 288 (35), 25362-25374. doi: 10.1074/jbc.M113.496281

  • Schroder, Kate, Irvine, Katharine M., Taylor, Martin S., Bokil, Nilesh J., Le Cao, Kim-Anh, Masterman, Kelly-Anne, Labzin, Larisa I., Semple, Colin A., Kapetanovic, Ronan, Fairbairn, Lynsey, Akalin, Altuna, Faulkner, Geoffrey J., Baillie, John Kenneth, Gongora, Milena, Daub, Carsten O., Kawaji, Hideya, McLachlan, Geoffrey J., Goldman, Nick, Grimmond, Sean M., Carninci, Piero, Suzuki, Harukazu, Hayashizaki, Yoshihide, Lenhard, Boris, Hume, David A. and Sweet, Matthew J. (2012). Conservation and divergence in Toll-like receptor 4-regulated gene expression in primary human versus mouse macrophages. Proceedings of the National Academy of Sciences of the USA, 109 (16), E944-E953. doi: 10.1073/pnas.1110156109

  • Roberts, Tara L., Idris, Adi, Dunn, Jasmyn A., Kelly, Greg M., Burnton, Carol M., Hodgson, Samantha, Hardy, Lani. L., Garceau, Valerie, Sweet, Matthew J., Ross, Ian L., Hume, David A. and Stacey, Katryn J. (2009). HIN-200 proteins regulate caspase activation in response to foreign cytoplasmic DNA. Science, 323 (5917), 1057-1060. doi: 10.1126/science.1169841

  • Sweet, Matthew J., Campbell, Carol C., Sester, David P., Xu, Damo, McDonald, Rebecca C., Stacey, Katryn J., Hume, David A. and Liew, Foo Y. (2002). Colony-stimulating factor-1 suppresses responses to CpG DNA and expression of toll-like receptor 9 but enhances responses to lipopolysaccharide in murine macrophages. Journal of Immunology, 168 (1), 392-399. doi: 10.4049/jimmunol.168.1.392

  • Sweet, M. J., Leung, B. P., Kang, D. W., Sogaard, M., Schulz, K., Trajkovic, V., Campbell, C. C., Xu, D. M. and Liew, F. Y. (2001). A novel pathway regulating lipopolysaccharide-induced shock by ST2/T1 via inhibition of toll-like receptor 4 expression. Journal of Immunology, 166 (11), 6633-6639. doi: 10.4049/jimmunol.166.11.6633

  • Stacey, K. J., Sweet, M. J. and Hume, D. A. (1996). Macrophages ingest and are activated by bacterial DNA. Journal of Immunology, 157 (5), 2116-2122.

Book Chapter

Journal Article

Conference Publication

Grants (Administered at UQ)

PhD and MPhil Supervision

Current Supervision

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Principal Advisor

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Principal Advisor

    Other advisors:

  • Doctor Philosophy — Associate Advisor

    Other advisors:

  • Doctor Philosophy — Associate Advisor

    Other advisors:

  • Doctor Philosophy — Associate Advisor

    Other advisors:

  • Doctor Philosophy — Associate Advisor

    Other advisors:

  • Doctor Philosophy — Associate Advisor

  • Doctor Philosophy — Associate Advisor

    Other advisors:

  • Doctor Philosophy — Associate Advisor

    Other advisors:

Completed Supervision

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • We have found that specific HDAC enzymes constrain macrophage antimicrobial responses, particularly TLR-inducible mitochondrial fission. This project will explore the specific molecular mechanisms by which HDACs constrain macrophage antimicrobial pathways and will investigate novel anti-infective approaches that target HDAC enzymes.

  • Projects are available to investigate different aspects of TLR-inducible inflammatory pathways in macrophages, for example the role of a novel TLR adaptor in macrophage inflammatory responses and HDAC-mediated control of metabolic pathways in macrophage-mediated inflammation.

  • Innate immune cells deliver toxic levels of zinc to invading microorganisms as an antimicrobial strategy, with zinc-sensitive mutants of a number of pathogens compromised for defence against innate immune cells. This project will focus on the cellular and molecular mechanisms involved in initiation of this host defence pathway.

  • In addition to controlling energy production, mitochondria are key regulators of macrophage inflammatory and antimicrobial responses. Lipid droplets, which interact with and regulate mitochondria, have also been linked to specific innate immune functions. This project will explore the control of macrophage inflammatory and antimicrobial responses by mitochondria and lipid droplets.

  • The circadian clock is a conserved gene regulatory network that synchronizes physiological processes with daily fluctuations in sleep/wake cycles. The circadian clock is also an important regulator of immune responses to infection, and this project would explore the mechanisms by which circadian rhythm influences innate immune inflammatory and antimicrobial responses.