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Benjamin Raymond

Summary
My research has primarily been focused on the elucidation of eukaryote responses to bacterial infection. As a researcher, my passion is to explore and decipher the diverse signalling events associated with bacterial infection as well as pathogenic effector molecules. I have skills in an array of multidisciplinary systems-wide techniques such as, proteomics, transcriptomics, and bioinformatic technologies that I have utilised to investigate the ability of bacteria to elicit responses from host cells and hijack numerous cellular processes. Additionally, I have a strong foundation in imaging, employing confocal microscopy, super resolution microscopy and electron microscopy to visually dissect these observations. 

Current Project
Deciphering the function(s) of the C-type lectin DCIR/CLEC4A 

Tuberculosis (TB), caused by the infectious agent Mycobacterium tuberculosis (Mtb), is a devastating disease and one of the leading causes of death in the developing world. Dendritic cells (DCs) play a key role in anti-mycobacterial immunity and express a range of pattern-recognition receptors which are involved in the recognition of Mtb antigens. The Neyrolles’ lab has characterised a number of these receptors, with the most recent being, and the focus of this project, the Dendritic Cell Immunoreceptor (DCIR). They have demonstrated that compared to wild-type mice, mice with a knockout in the DCIR homolog (mDCIR1) display increased antimycobacterial immunity as a result of an impaired response to type I interferon and an increased production of IL-12 in DCs. Consequently, mDCIR1-KO mice control Mtb better than their wild-type counterparts, but also develop increased lung inflammation. The aim of this project is to decipher the precise functions of DCIR in order to better understand its role in controlling the balance between type I and type II IFN responses; relevant not only in immunity to TB but in the greater context of a number of inflammatory diseases.


Short CV
Previous appointments

  • 2016 - 2018: Research Associate, ithree Institute, University of Technology Sydney, Australia
  • 2015 - 2015: Research Assistant, ithree Institute, University of Technology Sydney, Australia

Education

  • 2011 - 2015: PhD, Molecular Microbiology, University of Technology Sydney, Australia

            Thesis Title: Molecular interactions between Mycoplasma hyopneumoniae and host cells

  • 2010 - 2010: BSc (Honours, First Class), University of Technology Sydney, Australia

            Thesis Title: Proteomic analysis of biofilms formed by Mycoplasma hyopneumoniae, the causative agent of porcine enzootic pneumonia


Awards & Honours

  1. 2018: Recipient of a Marie Curie Individual Fellowship 
  2. 2016: Louis Dienes Postdoctoral Award, 21st Congress of the International Organisation for Mycoplasmology
  3. 2015: Student Oral Presentation Award, BacPath 13: Molecular Analysis of Bacterial Pathogens
  4. 2015: Australian Society for Microbiology NSW-ACT Branch Prize, Becton Dickinson Student Award Competition
  5. 2014: Student Poster Presentation Award, the 3rd International Prato Conference on 'The Pathogenesis of Bacterial Diseases of Animals'
  6. 2014: Student Oral Presentation Award, the 19th Lorne Proteomics Symposium
  7. 2011: Dean’s Merit List for Academic Excellence, University of Technology Sydney

 

Selected publications 

  1. Raymond, B.B., Madhkoor, R., Schleicher, I., Uphoff, C.C., Turnbull, L., Whitchurch, C.B., Rohde, M., Padula, M.P., and Djordjevic, S.P. (2018). Extracellular Actin Is a Receptor for Mycoplasma hyopneumoniae. Frontiers in cellular and infection microbiology 8, 54.
  2. Raymond, B.B., Jenkins, C., Seymour, L.M., Tacchi, J.L., Widjaja, M., Jarocki, V.M., Deutscher, A.T., Turnbull, L., Whitchurch, C.B., Padula, M.P., et al. (2015). Proteolytic processing of the cilium adhesin MHJ_0194 (P123J) in Mycoplasma hyopneumoniae generates a functionally diverse array of cleavage fragments that bind multiple host molecules. Cellular microbiology 17, 425-444.
  3. Raymond, B.B., and Djordjevic, S. (2015). Exploitation of plasmin(ogen) by bacterial pathogens of veterinary significance. Veterinary microbiology 178, 1-13.
  4. Raymond, B.B., Tacchi, J.L., Jarocki, V.M., Minion, F.C., Padula, M.P., and Djordjevic, S.P. (2013). P159 from Mycoplasma hyopneumoniae binds porcine cilia and heparin and is cleaved in a manner akin to ectodomain shedding. Journal of proteome research 12, 5891-5903.

 

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