Odilia Wijburg, PhD
|Academic Degrees||Contact Details|
|1993: BSc Utrecht University, The Netherlands
1997: PhD Free University, Amsterdam, The Netherlands
|Tel: +61 3 8344 9919
Fax: +61 3 8347 1540
Room 4.14B, Department of Microbiology and Immunology
1997-2000: Research Fellow, Department of Microbiology and Immunology, The University of Melbourne
2001-2004: NHMRC Peter Doherty Fellow, Department of Microbiology and Immunology, The University of Melbourne
2005-2006: C.R. Roper Fellow, Fac. Medicine, Dentistry and Health Sciences, The University of Melbourne
2007-present: NHMRC R.D. Wright Senior Research Fellow, Department of Microbiology and Immunology, The University of Melbourne
2007-present: A/Professor, The BioDesign Institute, Arizona State University, Tempe, AZ, USA
Odilia obtained her BSc degree from Utrecht University and her PhD degree from Free University in Amsterdam, The Netherlands. In 1997 she moved to Australia and joined the Department of Microbiology and Immunology at The University of Melbourne. Her research interests focus on host-pathogen interactions at the mucosal surface with emphasis on the interplay between host and poly-microbial infections. Her research has been recognized with prestigious awards, including NHMRC Peter Doherty Fellowship (2001) and R.D. Wright Fellowship (2007) and the Pfizer ‘Robert Austrian Award for Pneumococcal Vaccinology’ (2010).
Dr Wijburg is the President of Mucosal Immunology Special Interest Group of Australasian Society for Immunology. She also has a strong interest in undergraduate teaching and actively participates in teaching in 3rd year Science and Biomed Science subjects.
Streptococcus pneumoniae and influenza virus synergism, immunity to pneumococcal infections, mucosal immunity.
About 3 million annual deaths are due to Streptococcus pneumoniae, a bacterium that transiently colonises the mucosal surfaces of the human upper respiratory tract and is a leading etiological agent in otitis media, pneumonia, bacteremia and meningitis. In Australia, serious pneumococcal infections including otitis media (OM) are a major health problem, especially among the Indigenous Aboriginal population, with otitis media and meningitis rates that are reportedly the highest in the world and nasopharyngeal carrier state that reaches up to 80% within a few weeks after birth.
While transient colonisation with S. pneumoniae is normally asymptomatic, it is well known that a concurrent viral infection, such as influenza A virus, can affect the resistance to asymptomatic S. pneumoniae carriage. The overall aim of this theme is to further understand how influenza virus predisposes to pneumococcal disease, including otitis media and pneumonia, and S. pneumoniae transmission between individuals. Other, related research projects focus on determining the immune correlates of protection against S. pneumoniae infection.
Role of viral surface proteins in facilitating bacterial otitis media
Figure 1: Front cover of Journal of
Infectious Diseases, 13 Nov 2011.
Figure 3: Long-term colonization with
S. pneumoniae in infant mouse model. Cross
section through nasopharynx of infant mice
shows adherence of S. pneumoniae (red) to
epithelial cells and presence of GR-1+ cells
Otitis media is an inflammation of the middle ear that affects almost every child under the age of five and can lead to fatal meningitis or permanent hearing loss. Despite the prevalence of otitis media, our understanding of disease pathogenesis is limited. We recently developed a clinically relevant murine model of otitis media (Figure 1) and showed that co-infection of S. pneumoniae colonized mice with influenza A virus/Udorn/72 resulted in acute middle ear inflammation and bacterial outgrowth in the ear. Using a panel of influenza A virus strains, we now have evidence that the viral haemagglutinin facilitates pneumococcal otitis media and this correlates with the ability of the virus strain to infect middle ear epithelial cells and induce an inflammatory response. Our current research projects focus on understanding the molecular mechanisms of respiratory virus induced bacterial disease.
Immmunity to pneumococcal infections
Colonization with Sp results in development of immunity that protects against re-colonization, although the immunological correlates of protection are not well understood. Retrospective studies have shown that age-specific protection against Sp is not serotype specific and suggest that non-capsular pneumococcal antigens contribute to naturally acquired immunity against IPD. Currently licensed vaccines are based on polysaccharide antigens and have led to a reduction in IPD, however, the wide spread use of 7-valent polysaccharide-conjugate vaccine (7vPCV) has also been associated with a number of clinical problems, in particular ‘serotype replacement’ where the reduction in vaccine serotypes is accompanied by a relatively small but progressive increase in IPD caused by non-vaccine serotypes, including in healthy hosts. These data demonstrate that widespread vaccination has altered the dynamics of pneumococcal transmission, and this, together with the increasing number of (multiple) antibiotic resistant strains and the risk of ‘disease replacement’, will have significant clinical ramifications. Having established the first experimental model to study transmission of S. pneumonia (Figure 2, below) and a model to study long term colonization with S. pneumonia (Figure 3, right), we aim to identify mechanisms of immunity to S. pneumoniae and their protective effect against carriage and transmission of vaccine and non-vaccine S. pneumoniae serotypes.
|Figure 2: Using in vivo bioluminescence to visualize pneumococcal infection in infant mice.
Left hand panel show luminescence from animal colonized with
S. pneumoniae EF3030lux, middle and right hand panel show luminescence from animal co-infected with influenza A virus.
Nancy Wang (PhD student)
Kirsty Short (PhD student)
Mary John (PhD student)
Thian Ng (BSc (Hons) student)
Dr P Reading, Department of Microbiology and Immunology, The University of Melbourne
Dr T Brodnicki, St Vincents Research Institute, Melbourne
Dr S Bozinovski, Deptartment of Pharmacology, The University of Melbourne
Prof R Strugnell, Department of Microbiology and Immunology, The University of Melbourne
Dr A Walduck, RMIT University, Melbourne
Prof R Curtiss III, The BioDesign Institute, Arizona State University, Tempe, AZ, USA
- Kupz A, Juarda G, Gebhardt T, Sander LE, Short KR, Diavatopoulos DA, Wijburg OL, Cao H, Waithman JC, Chen W, Fernandez-Ruiz D, Whitney PG, Heath WR, Curtiss R 3rd, Tschopp J, Strugnell RA, Bedoui S. NLRC4 inflammasomes in dendritic cells regulate noncognate effector function by memory CD8(+) T cells. Nat Immunol 2012; 13: 162-169.
- KR Short, DA Diavatopoulos, R Thorton, J Pedersen, RA. Strugnell, AK Wise, PC Reading, Wijburg, OLC. Influenza virus induces bacterial and non-bacterial otitis media. J Inf Dis 2011; 204: 1857-1865.
- Wilksch JJ, Clements A, Gabbe JL, Short KR, Cao H, Cavaliere R, James CE, Whitchurch CB, Schembri MA, Chuah MLC, Liang Z-X, Wijburg OLC, Jenney AW, Lithgow T, Strugnell RA. MrkH, a novel c-di-GMP-dependent transcriptional activator, controls Klebsiella pneumoniae biofilm formation by regulating type 3 fimbriae expression. PLoS Path 2011; 7: e1002204.
- Wang N, Strugnell RA, Wijburg OLC, Brodnicki T. Measuring bacterial load and immune cells in mice infected with Listeria monocytogenes. J Vis Exp 2011; 54 DOI 10: 3791/3076.
- Short KR, Diavatopoulos DA, Reading PC, Brown LE, Rogers K, Strugnell RA, Wijburg OLC. Using bioluminescent imaging to investigate synergism between Streptococcus pneumoniae and influenza A virus in infant mice. J Vis Exp 2011; 50; DOI 10. 3791/2357.
- Becher D, Deutscher ME, Simpfendorfer KR, Wijburg OLC, Pederson JS, Lew AM, Strugnell RA, Walduck AK. Local recall responses in the stomach involving reduced regulation and expanded help mediate vaccine-induced protection against Helicobacter pylori in mice. Eur J Immunol 2010; 40: 2778-2790.
- Achard MES, Tree JJ, Holden JA, Simpfendorfer KR, Wijburg OLC, Strugnell RA, Schembri MA, Sweet MJ, Jennings MP, McEwan AG. The multi-copper oxidase CueO of Salmenella enterica serovar Typhimurium is required for systemic virulence. Infect Immun 2010; 78: 2312-2319.
- Bedoui S, Kupz A, Wijburg OL, Walduck AK, Rescigno M, Strugnell RA. Different bacterial pathogens, different strategies, yet the aim is the same: evasion of intestinal dendritic cells recognition. J Immunol 2010; 184: 2237-2242.
- Diavatopoulos DA, Short KR, Price JT, Wilksch JJ, Brown LE, Briles DE, Strugnell RA, Wijburg OL. Influenza A virus facilitates Streptococcus pneumoniae transmission and disease. FASEB J 2010; 24; 1789-1798.
- Strugnell RA, Wijburg OLC. Role of secretory antibodies in protection against infection. Nature Reviews Microbiology 2010; 8: 656-667.
- De Kauwe AL, Chen Z, Anderson RP, Keech CL, Price JD, Wijburg OLC, Jackson DC, Ladhams J, Allison J, McCluskey J. Resistance to coeliac disease in humanized HLA-DR3-DQ2-transgenic mice expressing specific anti-gliadin CD4+ T cells. J Immunol 2009; 182: 7440-7450.