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- A multi-pronged approach to targeting myeloproliferative neoplasms
- A new paradigm of machine learning-based structural variant detection
- A whole lot of junk or a treasure trove of discovery?
- Advanced imaging interrogation of pathogen induced NETosis
- Analysing the metabolic interactions in brain cancer
- Atopic dermatitis causes and treatments
- Boosting the efficacy of immunotherapy in lung cancer
- Building a cell history recorder using synthetic biology for longitudinal patient monitoring
- Characterisation of malaria parasite proteins exported into infected liver cells
- Deciphering the heterogeneity of the tissue microenvironment by multiplexed 3D imaging
- Defining the mechanisms of thymic involution and regeneration
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- How do nutrition interventions and interruption of malaria infection influence development of immunity in sub-Saharan African children?
- Human lung protective immunity to tuberculosis
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- Integrative analysis of single cell RNAseq and ATAC-seq data
- Interaction with Toxoplasma parasites and the brain
- Interactions between tumour cells and their microenvironment in non-small cell lung cancer
- Investigation of a novel cell death protein
- Malaria: going bananas for sex
- Mapping spatial variation in gene and transcript expression across tissues
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- Multi-modal computational investigation of single-cell communication in metastatic cancer
- Nanoparticle delivery of antibody mRNA into cells to treat liver diseases
- Naturally acquired immune response to malaria parasites
- Organoid-based discovery of new drug combinations for bowel cancer
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- Removal of tissue contaminations from RNA-seq data
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- Role of glycosylation in malaria parasite infection of liver cells, red blood cells and mosquitoes
- Screening for novel genetic causes of primary immunodeficiency
- Single-cell ATAC CRISPR screening – Illuminate chromatin accessibility changes in genome wide CRISPR screens
- Spatial single-cell CRISPR screening – All in one screen: Where? Who? What?
- Statistical analysis of single-cell multi-omics data
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- Using combination immunotherapy to tackle heterogeneous brain tumours
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- Using structural biology to understand programmed cell death
- Validation and application of serological markers of previous exposure to malaria
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Inflammation

Inflammation is an early defense that protects our body from infection. However, ongoing or misdirected inflammation underlies many diseases.
Our researchers are revealing how inflammation is controlled, and advancing the diagnosis and treatment of inflammatory diseases.
Our inflammation research
Our researchers seek to understand how inflammation is controlled in health and disease. To do this they are investigating:
- The molecules and cells that contribute to the initiation, magnitude and resolution of inflammatory responses.
- Inflammatory pathways that are associated with disease.
- New strategies to treat harmful inflammation, and promote beneficial inflammation.
The goal of our inflammation research is to advance strategies to diagnose, treat and prevent inflammatory diseases including:
- Coeliac disease
- Inflammatory bowel disease
- Lupus
- Multiple sclerosis
- Rheumatic fever
- Rheumatoid arthritis
- Type 1 diabetes
- Infections including influenza and malaria
- Cancers associated with inflammation such as bowel cancer and stomach cancer
What is inflammation
Inflammation is the body’s natural response to infection, disease and tissue damage. Inflammation is driven by immune cells, and also serves to heighten the immune response.
Features of inflamed tissues include:
- Redness and warmth, from increased blood flow to the area.
- Swelling, from an influx of fluid.
- Pain.
- Immobility.
These symptoms of inflammation serve several important functions:
- Alerting and attracting immune cells to an area of potential infection.
- Releasing substances that help to repair damaged tissue.
- Immobilising the injured or infected tissue to reduce damage or spread of infection.
Inflammation can be acute, meaning it is rapidly resolved, or chronic, meaning it can persist for years.
What causes inflammation?
Inflammation can have a variety of triggers including:
- Tissue damage, such as a burn or cut.
- Clot formation by platelets.
- The presence of a foreign substance.
- Microbial infection.
- Some forms of cell death.
Inflammation begins with innate immune cells, such as neutrophils, being alerted to the trigger. This may be because damaged tissue has released ‘alert’ signals, or because the immune cell has detected microbial molecules such as bacterial cell wall components.
When activated, innate immune cells can immediately release a variety of inflammatory substances. These substances trigger the features of inflammation in nearby tissue, protecting the site and attracting an influx of additional immune cells. Different immune cell types, and inflammatory mediators are detected in acute and chronic inflammation.
Inflammatory mediators are typically short-lived. This serves to limit the duration of an inflammatory response. As soon as the trigger is removed, inflammation will normally diminish, preventing tissue damage.
Inflammation and cell death
Our research into how cells die has revealed that many of the molecules contributing to cell death have dual roles in inflammation, or are closely related to molecules functioning in inflammatory pathways.
Some types of cell death trigger inflammation. This ensures that the abnormal death of cells alerts immune cells to a potentially dangerous situation.
Beneficial inflammation
Inflammation is an important component of the innate immune response, which is the body’s first line of defense against infection. Inflammatory mediators enhance the responses of immune cells to potential infections, by:
- Increasing blood flow and movement of immune cells into the inflamed tissue
- Stimulating immune cells, such as triggering macrophages to be more likely to engulf nearby substances.
- Stimulating production of new immune cells through the release of colony stimulating factors
Inflammation is important for the generation of protective immunological memory. This ensures that repeat exposures to a microbe are rapidly dealt with by established immune cells that recognise the infectious agent.
Most vaccines include substances that trigger inflammation. These contribute to better immune responses, and longer-lasting immune protection.
Inflammatory diseases
Excessive or ongoing inflammation can cause pain and tissue damage, and prevent the normal functioning of the body’s organs.
Short-term, acute inflammation can be responsible for many of the symptoms of infections. These symptoms, such as fever, tend to assist the immune clearance of infection. Excessive or misplaced acute inflammation can cause severe illness or death.
Chronic inflammation is also associated with many diseases. Approximately one in three Australians has a chronic inflammatory disease, such as rheumatoid arthritis. These diseases place a significant social and economic burden on the community.
Chronic inflammation is triggered by ongoing immune responses. These immune responses can be against:
- A chronic infection that is not cleared. Chronic inflammation to the hepatitis B virus contributes to liver damage.
- The body’s own tissue, such as joint tissue in rheumatoid arthritis.
In some conditions, such as rheumatic fever, inflammation begins in response to an infection by Streptococcus bacteria, but is redirected later to heart tissue, causing damage.
Treating inflammation
In many inflammatory diseases, symptoms can be greatly reduced in the short term by appropriate treatment. These include:
- Corticosteroids that reduce immune cell function.
- ‘Non-steroidal’ anti-inflammatory medications that interfere with key molecules or cells contributing to the symptoms of inflammation.
- Targeted therapies that specifically inhibit the molecules that underpin inflammation or immune cell function. These are showing great promise in improving the outlook for people with inflammatory diseases.
Compressing, immobilising and cooling the inflamed area can also improve the symptoms of inflammation, but do not eliminate the underlying cause of the inflammation.
Researchers:
WEHI.TV animation: how insulin is normally produced in the body and how its production is destroyed in type 1 diabetes.
Dr Tracy Putoczki presents her research findings into targeting cytokines in inflammatory diseases with a focus on Interkeukin-11.
Our research has revealed the structure of a protein that triggers a form of programmed cell death called necroptosis
Our public forum explained how research into arthritis is leading to better treatments.
While most proteins were readily consumed, some people’s immune systems struggled to tolerate others.