Gastroenterology, Immunology and Neuroscience

Gastroenterology, Immunology and Neuroscience (GIN) Discovery Program

The Gastroenterology, Immunology and Neuroscience Discovery Program is a transdisciplinary consortium working to improve our understanding of the gut-immune-brain axis and to create solutions to combat complex health conditions.

Historically medical research has focused on individual organs or systems; however, it is becoming clear that by taking this siloed approach we fail to see the bigger health picture. We now know that health conditions such as allergies, diabetes, epilepsy, and Crohn’s disease are not conditions of only one system but are due to a combination of factors affected by the “gut-immune-brain axis”. The gut-immune-brain axis refers to interactions between the gastrointestinal system, the immune system and the brain / central nervous system. With experts in Gastroenterology, Immunology  and Neuroscience, we've positioned itself to tackle this new frontier in translational research.

Connect with the GIN Discovery Program
Twitter:   @GIN_Discovery

Who we are

The program consists of over 80 world-class scientists and clinicians who are passionate about improving our understanding of conditions of the gut-immune-brain axis and finding better ways to manage and prevent these complex conditions.

The executive team

Research themes

Special interest groups

Our special interest groups provide an opportunity for our members to identify and focus on specific areas of research.

The Pitch

The Pitch supports collaborative research between early and mid-career researchers that contributes to our understanding of the gut-immune-brain axis. Successful projects receive up to $25,000 to support novel research projects.

The Pitch funded projects for 2022

Can we treat concussion by restricted feeding? Exploring the gut-brain axis during brain injury

Glenn Yamakawa & Aidil Zaini

Concussion is a highly prevalent injury, particularly occurring in adolescence. These head injuries are known to cause inflammation in the brain. Given brain development is crucial during these formative years, the consequences of concussion may be serious and long-lasting. Although inflammation starts in the brain, the gut can also be impacted. The connection between the gut and the brain is referred to as the gut-brain axis. Due to an increasingly 24-hour society and widespread artificial lighting, productivity, or social activities can now occur at all times of the day or night. Similarly, in many modern societies, food is readily available around the clock. Unfortunately, these 24-hour societies are not compatible with the environments in which all living creatures evolved. The overarching goal of this study is to determine whether modifying the feeding regime can promote a healing response to reduce concussion-induced inflammation in both the brain and the gut. We hope to harness these dietary interventions as a potential treatment for brain injury.

Can we prevent severe epilepsy by limiting peripheral inflammation?

Idrish Ali & Evelyn Tsantikos

Multiple studies have shown that inflammation in the brain plays a critical role in the development of epilepsy. It has also been shown that inflammation elsewhere in the body can feed back into the brain via the bloodstream and worsen epilepsy outcomes. By applying this knowledge to the study of a known growth factor which is involved in the regulation of peripheral myeloid cells that can promote chronic inflammatory disease in other settings, we propose that the loss of this factor alters peripheral and brain immune responses and will evaluate its potential for therapeutic targeting in epilepsy.

Developing the first Australian mouse model of anti-NMDAR autoimmune encephalitis

Matt Hudson, Zoe Ding & Robb Wesselingh

Autoimmune encephalitis (AE) constitutes a group of inflammatory brain conditions, presenting with seizures, cognitive deficits, and mood/behavioural alterations. Up to 50% of the AE cases are associated with the presence of antibodies in the patient's cerebrospinal fluid which target neuronal proteins, with antibodies against the N-methyl-D-aspartate (NMDA) receptor (NMDAR) being the most common. However, the pathogenic mechanism of those antibodies is not well-understood, largely due to the lack of valid animal models. In this proposal, we aim to establish a mouse model of AE by administering anti-NMDAR antibodies directly to the mouse brain and we will assess behavioural and immunological changes during the disease development. This project will form the basis for pursuing long-term goals in identification of the pathogenic NMDAR epitopes responsible for disease, exploring how systemic antibodies enter the brain to cause disease, and development and testing of novel, targeted therapeutics.