Register      Login
Microbiology Australia Microbiology Australia Society
Microbiology Australia, bringing Microbiologists together
RESEARCH ARTICLE (Open Access)

Munching microbes: diet–microbiome interactions shape gut health and cancer outcomes

Emma Todd A , Reem Elnour A * , Rebecca Simpson B * , Miguel Castaneda C * and Erin R Shanahan A D
+ Author Affiliations
- Author Affiliations

A School of Life and Environmental Sciences, Charles Perkins Centre, University of Sydney, Camperdown, NSW, Australia

B Melanoma Institute Australia, Charles Perkins Centre, University of Sydney, Camperdown, NSW, Australia

C School of Medical Sciences, Charles Perkins Centre, University of Sydney, Camperdown, NSW, Australia

D Tel.: +61 2 8627 7113; Email: erin.shanahan@sydney.edu.au

Microbiology Australia 42(2) 60-64 https://doi.org/10.1071/MA21026
Submitted: 30 March 2021  Accepted: 20 May 2021   Published: 17 June 2021

Journal Compilation © The Authors 2021 Open Access CC BY-NC-ND, published (by CSIRO Publishing) on behalf of the ASM

Abstract

The gut microbiome describes the complex community of microorganisms that populate the gastrointestinal tract. Gut microbes in the large bowel utilise both dietary-derived nutrients, such as host-indigestible carbohydrates (fibre) and excess protein, host-derived nutrients (intestinal mucin), and also interact with the by-products of digestion such as bile acids. They transform these compounds into a series of metabolites that can profoundly shape host physiology both locally and systemically. These metabolites can fundamentally alter host outcomes, promoting either gut health, or sub-optimal conditions in the gut that contribute to poor health, including increased risk of cancer. The microbiome of an individual has also been shown to impact response to cancer treatment strategies, including both treatment efficacy and side-effects in the gut and more systemically. This makes the microbiome a powerful potential tool for therapeutic purposes, once we overcome the challenges associated with individual variation in microbial community composition. As the gut microbial ecosystem is primarily altered by nutrient availability, diet therefore represents an important asset in therapeutically altering the gut microbiome.

Consumption of a sub-optimal, Western-style diet (WD) – containing proteins from processed meats, saturated fats, refined grains and sugars, while lacking plant-derived, fibre-containing components1 – has been identified as a key driver of various disadvantageous health states such as colorectal cancer (CRC)24, obesity5, Crohn’s disease6, and irritable bowel syndrome (IBS)7. Researchers have been seeking to understand the mechanisms behind these significant associations, including the impact of diet on the microbiome and the relationship between gut microbes and their host, particularly the epithelial barrier.

When examining the relationship between diet and the gut microbiome it is important to consider the nature of the gut environment and nutrient availability from the perspective of microbes. After digestion and absorption in the small intestine (Figure 1), the nutrients available to microbes in the large bowel are those unable to be digested by host enzymes, those surplus to requirements, or derived from host cells. Different microorganisms will have varying preferences and capabilities for consumption of dietary or host-derived carbohydrates and proteins8,9. Interactions between nutrients and the ratios of macronutrients available are also important in favouring the growth of microbes with particular nutritional strategies10. Therefore, in the context of the large bowel, which is the primary site of microbial fermentation in the gut, overall dietary intake will shape microbial community composition.


Figure 1.  Digestive processes and microbial metabolism in the small and large intestine. Digestion and absorption of monosaccharides, amino acids and lipids occurs in the small intestine. Host-indigestible carbohydrates (fibre), along with unabsorbed nutrients and by-products of digestion pass into the large intestine where the majority of gut microbes are present. Microbial metabolic processes in the large bowel results in a variety of metabolites that can be beneficial or detrimental for gut health.
Click to zoom

The intestinal epithelium and mucosal layer is a key site of interaction between the host, dietary nutrients and gut microbes11. It is a physical and immunological barrier and plays a fundamental role in the maintenance of host health and disease prevention. The layer of epithelial cells separates the luminal contents of the gut, including microbes, from the underlying tissue12. The epithelial layer itself is protected by a mucin layer, which prevents direct contact with microbial cells (Figure 2). A number of microbes are able to cleave mucin molecules and therefore gut microbe-mediated mucin turnover is part of healthy gut function13.


Figure 2.  Dietary intake and nutrient availability shapes the balance between pro and anti-inflammatory properties of the gut microbiome. (A) In healthy, high fibre environment, microbes will degrade complex carbohydrates resulting in SCFA production. Healthy mucin turnover occurs through interaction with mucin degrading microbes. Optimal intestinal barrier function and immune regulation are favoured. (B) In diets lacking dietary fibre, and high in fats and/or protein, there is reduced production of beneficial short chain fatty acids, degradation of the mucin layer through excess microbial degradation, and production of potentially detrimental metabolites. This can result in increased permeability of the intestinal barrier leading to inflammation and excess proliferation of epithelial cells.
Click to zoom

One consequence of fibre-deprived diets such as the WD is decreased abundance of fibre-degrading microbes, and their beneficial metabolites, including short chain fatty acids (SCFAs) such as butyrate, acetate and propionate. SCFAs are key microbial metabolites involved in immune regulation and gut barrier integrity. While butyrate and propionate are dominantly utilised locally in the gut or liver, acetate can readily be detected in systemic circulation suggesting that it could also modulate immune function at more distant sites. These SCFAs can bind to key receptors including GPR43 and GPR109A on intestinal epithelial cells, which promotes epithelial barrier repair and turnover via NLRP3 inflammasome activation14,15. Butyrate is also the primary energy source for epithelial cells and is vital in modulating host immune responses14,16 and maintains the epithelial barrier by decreasing epithelial permeability through upregulating tight junction proteins (Figure 2), including zonula occludens protein 1 and members of the claudin protein family17. SCFAs can also promote the differentiation and accumulation of regulatory T-cells (Treg) in the gut, central to the maintenance of immune tolerance18,19.

While fibre is the dominant dietary-derived nutrient source in the large intestine, some microbes are able to utilise glycoprotein-rich mucins as an alternative energy source20, including Akkermansia mucinophila and members of the Bacteroides genus13. Mucin turnover is critical for maintaining intestinal integrity, although a tight balance between mucus degradation and renewal is required, with an essential role for mucin-degrading microbes. However, fibre-deprived environments select for microbes with the ability to utilise mucins, and can lead to excessive degradation of the mucus layer exposing the underlying epithelial cells to luminal antigen, promoting inflammatory responses (Figure 2). Furthermore, as mucin is an endogenous source of sulfur, an additional outcome of excessive mucin degradation is increased production of hydrogen sulfide (H2S) by sulfate-reducing bacteria such as Bilophila spp. and Desulfovibrio spp. H2S is a genotoxic compound that has been shown to damage DNA and trigger chromosomal instability21.

Increased levels of primary bile acids are also associated with the WD, required for emulsification of dietary fat (Figure 1). While much of the bile acid pool is reabsorbed in the ileum, bile acids are subject to extensive microbial metabolism including deconjugation of amino acids taurine and glycine, and conversion to secondary bile acids (SBAs)22. Certain SBAs such as 3-oxolithocholic acid and isoallolithocholic acid have immunomodulatory properties, inhibiting the generation of T helper 17 cells and promoting the differentiation of regulatory T cells respectively23. The SBA 3β-hydroxydeoxycholic acid also shapes the gut immune response by inhibiting the ability of dendritic cells to activate adaptive immune cells, leading to an increase in regulatory T cells in the colon24. Activation of the bile acid receptor TGR5/GPBAR1 has also been shown to promote macrophage polarisation towards the anti-inflammatory M2 phenotype, and reduce the expression of inflammatory genes in a mouse model of colitis25. The immunoregulatory effects of these SBAs may be beneficial in mitigating inflammatory bowel diseases, and may help to prevent the development of colorectal cancer. However, other microbe-transformed bile acids such as deoxycholic and lithocholic acid have pro-carcinogenic properties (Figure 2) and predominantly act via the downregulation of p53, a tumour suppressor gene, and the generation of ROS to induce DNA damage and genomic instability, eventually resulting in increased cell proliferation26,27. Furthermore, during SBA production, sulfur-containing taurine is available for H2S generation22.

Therefore, the synergistic effect of the removal of fibre and high levels of saturated fat in the diet, as seen in the WD, can lead to reduced epithelial barrier function, erosion of the mucosal layer, inflammation and an increased susceptibility to luminal pathogens and carcinogens. The altered nutrient availability can also result in unfavourable gut microbiome compositions that have the potential to drive inflammation within the gut, therefore resulting in poor gut health.

In addition to inflammation-associated disorders of the gut such as IBD, these impacts on the gut epithelium are relevant to both local and systemic cancer outcomes. Locally, colorectal cancer (CRC) is linked to long term consumption of a WD28. CRC risk is determined by complex diet–microbe interactions, where the production of toxic microbial metabolites are capable of driving pro-carcinogenic responses that transform the epithelium29. In addition, increased epithelial permeability permeability – often referred to as ‘leaky gut’ (Figure 2) – enables the translocation of luminal antigens across the epithelium, promoting a local inflammatory response, while disruption to the mucus layer exposes stem cells to microbial metabolites that promote cell replication30. The outcome is uncontrolled proliferation of epithelial cells, resulting in tumour formation. However, predicting which individuals are most at risk of CRC development remains a challenge and further understanding of individual microbiome profiles, and how these interact with dietary intake, is required.

More recently, systemic impacts of the gut microbiome in the context of cancer immunotherapy distal to the gut have been identified. Immunotherapy acts to induce the immune system to target and eliminate cancer cells and has been used in various cancers including melanoma, lung and renal tumours3133. Emerging evidence indicates that higher fibre consumption is associated with improved response rates to therapy34, and the microbiome represents a promising target to overcome therapeutic resistance35 and reduce side-effects such as colitis36. While the specific taxa linking response to treatment across cohorts lack consensus3133, shared functional properties such as fibre fermentation and mucin turnover that support intestinal epithelial barrier integrity may be the underlying common features. However, whether fibre supplementation will be effective at modulating the microbiome in a feasible timeframe to improve treatment responses requires further investigation.

Although diet is well established to shape the composition of the microbiome, how an individual responds to a particular dietary intervention is dependent on the composition of an individual’s baseline microbiome. For example, individuals have been shown to respond differently to supplementation with the same type of fibre37,38. This has been linked to interspecies competition and functional redundancy within microbiome39. Inter-individual variation therefore presents a significant challenge in terms of designing effective therapeutic dietary interventions, as variable responses dependent on the assemblage of the microbiome would be expected. Additionally, different types of fibre are known to have different prebiotic effects, for example, not all fibre sources are equally capable of stimulating SCFA production40,41. Given the impact of inter-individual variation impact of an individual’s baseline microbiome a ‘one-size fits all’ approach will likely be ineffective, rather more personalised approaches will be necessary to enhance the reproducibility and success of nutritional interventions in the clinic.

While a significant body of research has emerged in this area, there remains much to be understood. What mechanisms underly the various host–microbe interactions at the epithelial interface, in response to different diets, in a clinical setting? How do individual gut environments and microbial ecosystems impact responses to treatments such as immunotherapy? Can tools be created to predict and modulate these outcomes? Understanding these issues could enable the implementation of personalised medicine, where the individual’s native microbiome, genetics, and dietary history could be considered prior to implementation of medical interventions, resulting in greater treatment effectiveness and fewer side-effects.


Conflicts of interest

The authors declare no conflicts of interest.


Declaration of funding

This research did not receive any specific funding.



References

[1]  Statovci, D. et al. (2017) The impact of Western diet and nutrients on the microbiota and immune response at mucosal interfaces. Front. Immunol. 8, 838.
The impact of Western diet and nutrients on the microbiota and immune response at mucosal interfaces.Crossref | GoogleScholarGoogle Scholar | 28804483PubMed |

[2]  Tayyem, R.F. et al. (2015) Macro- and micronutrients consumption and the risk for colorectal cancer among Jordanians. Nutrients 7, 1769–1786.
Macro- and micronutrients consumption and the risk for colorectal cancer among Jordanians.Crossref | GoogleScholarGoogle Scholar | 25763533PubMed |

[3]  Chun, Y.J. et al. (2015) Associations of colorectal cancer incidence with nutrient and food group intakes in Korean adults: a case-control study. Clin. Nutr. Res. 4, 110–123.
Associations of colorectal cancer incidence with nutrient and food group intakes in Korean adults: a case-control study.Crossref | GoogleScholarGoogle Scholar | 25954732PubMed |

[4]  Liu, L. et al. (2011) Is dietary fat associated with the risk of colorectal cancer? A meta-analysis of 13 prospective cohort studies. Eur. J. Nutr. 50, 173–184.
Is dietary fat associated with the risk of colorectal cancer? A meta-analysis of 13 prospective cohort studies.Crossref | GoogleScholarGoogle Scholar | 20697723PubMed |

[5]  Sonnenburg, J.L. and Backhed, F. (2016) Diet-microbiota interactions as moderators of human metabolism. Nature 535, 56–64.
Diet-microbiota interactions as moderators of human metabolism.Crossref | GoogleScholarGoogle Scholar | 27383980PubMed |

[6]  Gibson, P.R. and Shepherd, S.J. (2005) Personal view: food for thought--western lifestyle and susceptibility to Crohn’s disease. The FODMAP hypothesis. Aliment. Pharmacol. Ther. 21, 1399–1409.
Personal view: food for thought--western lifestyle and susceptibility to Crohn’s disease. The FODMAP hypothesis.Crossref | GoogleScholarGoogle Scholar | 15948806PubMed |

[7]  Marsh, A. et al. (2016) Does a diet low in FODMAPs reduce symptoms associated with functional gastrointestinal disorders? A comprehensive systematic review and meta-analysis. Eur. J. Nutr. 55, 897–906.
Does a diet low in FODMAPs reduce symptoms associated with functional gastrointestinal disorders? A comprehensive systematic review and meta-analysis.Crossref | GoogleScholarGoogle Scholar | 25982757PubMed |

[8]  Koropatkin, N.M. et al. (2012) How glycan metabolism shapes the human gut microbiota. Nat. Rev. Microbiol. 10, 323–335.
How glycan metabolism shapes the human gut microbiota.Crossref | GoogleScholarGoogle Scholar | 22491358PubMed |

[9]  Reese, A.T. et al. (2018) Microbial nitrogen limitation in the mammalian large intestine. Nat. Microbiol. 3, 1441–1450.
Microbial nitrogen limitation in the mammalian large intestine.Crossref | GoogleScholarGoogle Scholar | 30374168PubMed |

[10]  Holmes, A.J. et al. (2017) Diet–microbiome interactions in health are controlled by intestinal nitrogen source constraints. Cell Metab. 25, 140–151.
Diet–microbiome interactions in health are controlled by intestinal nitrogen source constraints.Crossref | GoogleScholarGoogle Scholar | 27889387PubMed |

[11]  Hamilton, M.K. et al. (2015) Changes in intestinal barrier function and gut microbiota in high-fat diet-fed rats are dynamic and region dependent. Am. J. Physiol. Gastrointest. Liver Physiol. 308, G840–G851.
Changes in intestinal barrier function and gut microbiota in high-fat diet-fed rats are dynamic and region dependent.Crossref | GoogleScholarGoogle Scholar | 25747351PubMed |

[12]  Odenwald, M.A. and Turner, J.R. (2017) The intestinal epithelial barrier: a therapeutic target? Nat. Rev. Gastroenterol. Hepatol. 14, 9–21.
The intestinal epithelial barrier: a therapeutic target?Crossref | GoogleScholarGoogle Scholar | 27848962PubMed |

[13]  Tailford, L.E. et al. (2015) Mucin glycan foraging in the human gut microbiome. Front. Genet. 6, 81.
Mucin glycan foraging in the human gut microbiome.Crossref | GoogleScholarGoogle Scholar | 25852737PubMed |

[14]  Singh, N. et al. (2014) Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis. Immunity 40, 128–139.
Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis.Crossref | GoogleScholarGoogle Scholar | 24412617PubMed |

[15]  Macia, L. et al. (2015) Metabolite-sensing receptors GPR43 and GPR109A facilitate dietary fibre-induced gut homeostasis through regulation of the inflammasome. Nat. Commun. 6, 6734.
Metabolite-sensing receptors GPR43 and GPR109A facilitate dietary fibre-induced gut homeostasis through regulation of the inflammasome.Crossref | GoogleScholarGoogle Scholar | 25828455PubMed |

[16]  Canani, R.B. et al. (2011) Potential beneficial effects of butyrate in intestinal and extraintestinal diseases. World J. Gastroenterol. 17, 1519–1528.
Potential beneficial effects of butyrate in intestinal and extraintestinal diseases.Crossref | GoogleScholarGoogle Scholar | 21472114PubMed |

[17]  Wang, K. et al. (2019) Claudin-7 downregulation induces metastasis and invasion in colorectal cancer via the promotion of epithelial-mesenchymal transition. Biochem. Biophys. Res. Commun. 508, 797–804.
Claudin-7 downregulation induces metastasis and invasion in colorectal cancer via the promotion of epithelial-mesenchymal transition.Crossref | GoogleScholarGoogle Scholar | 30528239PubMed |

[18]  Furusawa, Y. et al. (2013) Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. Nature 504, 446–450.
Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells.Crossref | GoogleScholarGoogle Scholar | 24226770PubMed |

[19]  Smith, P.M. et al. (2013) The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis. Science 341, 569–573.
The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis.Crossref | GoogleScholarGoogle Scholar | 23828891PubMed |

[20]  Desai, M.S. et al. (2016) A dietary fiber-deprived gut microbiota degrades the colonic mucus barrier and enhances pathogen susceptibility. Cell 167, 1339–1353.e21.
A dietary fiber-deprived gut microbiota degrades the colonic mucus barrier and enhances pathogen susceptibility.Crossref | GoogleScholarGoogle Scholar | 27863247PubMed |

[21]  O’Keefe, S.J.D. (2016) Diet, microorganisms and their metabolites and colon cancer. Nat. Rev. Gastroenterol. Hepatol. 13, 691–706.
Diet, microorganisms and their metabolites and colon cancer.Crossref | GoogleScholarGoogle Scholar |

[22]  Ridlon, J.M. et al. (2016) Consequences of bile salt biotransformations by intestinal bacteria. Gut Microbes 7, 22–39.
Consequences of bile salt biotransformations by intestinal bacteria.Crossref | GoogleScholarGoogle Scholar | 26939849PubMed |

[23]  Hang, S. et al. (2019) Bile acid metabolites control TH17 and Treg cell differentiation. Nature 576, 143–148.
Bile acid metabolites control TH17 and Treg cell differentiation.Crossref | GoogleScholarGoogle Scholar | 31776512PubMed |

[24]  Campbell, C. et al. (2020) Bacterial metabolism of bile acids promotes generation of peripheral regulatory T cells. Nature 581, 475–479.
Bacterial metabolism of bile acids promotes generation of peripheral regulatory T cells.Crossref | GoogleScholarGoogle Scholar | 32461639PubMed |

[25]  Biagioli, M. et al. (2017) The bile acid receptor GPBAR1 regulates the M1/M2 phenotype of intestinal macrophages and activation of GPBAR1 rescues mice from murine colitis. J. Immunol. 199, 718–733.
The bile acid receptor GPBAR1 regulates the M1/M2 phenotype of intestinal macrophages and activation of GPBAR1 rescues mice from murine colitis.Crossref | GoogleScholarGoogle Scholar | 28607110PubMed |

[26]  Bernstein, H. et al. (2005) Bile acids as carcinogens in human gastrointestinal cancers. Mutat. Res. Rev. Mutat. Res. 589, 47–65.
Bile acids as carcinogens in human gastrointestinal cancers.Crossref | GoogleScholarGoogle Scholar |

[27]  Cao, H. et al. (2014) The secondary bile acid, deoxycholate accelerates intestinal adenoma–adenocarcinoma sequence in Apc min/+ mice through enhancing Wnt signaling. 13, 563–571.
| 25106466PubMed |

[28]  O’Keefe, S.J.D. et al. (2015) Fat, fibre and cancer risk in African Americans and rural Africans. 6, 6342.

[29]  Gagnière, J. et al. (2016) Gut microbiota imbalance and colorectal cancer. World J. Gastroenterol. 22, 501–518.
Gut microbiota imbalance and colorectal cancer.Crossref | GoogleScholarGoogle Scholar | 26811603PubMed |

[30]  Kaiko, G.E. et al. (2016) The colonic crypt protects stem cells from microbiota-derived metabolites. Cell 165, 1708–1720.
The colonic crypt protects stem cells from microbiota-derived metabolites.Crossref | GoogleScholarGoogle Scholar | 27264604PubMed |

[31]  Gopalakrishnan, V. et al. (2018) Gut microbiome modulates response to anti-PD-1 immunotherapy in melanoma patients. Science 359, 97–103.
Gut microbiome modulates response to anti-PD-1 immunotherapy in melanoma patients.Crossref | GoogleScholarGoogle Scholar | 29097493PubMed |

[32]  Matson, V. et al. (2018) The commensal microbiome is associated with anti-PD-1 efficacy in metastatic melanoma patients. Science 359, 104–108.
The commensal microbiome is associated with anti-PD-1 efficacy in metastatic melanoma patients.Crossref | GoogleScholarGoogle Scholar | 29302014PubMed |

[33]  Routy, B. et al. (2018) Gut microbiome influences efficacy of PD-1-based immunotherapy against epithelial tumors. Science 359, 91–97.
Gut microbiome influences efficacy of PD-1-based immunotherapy against epithelial tumors.Crossref | GoogleScholarGoogle Scholar | 29097494PubMed |

[34]  Spencer, C.N. et al. (2019) Abstract 2838: The gut microbiome (GM) and immunotherapy response are influenced by host lifestyle factors. Cancer Res. 79, 2838.

[35]  Simpson, R.C. et al. (2021) Targeting the microbiome to overcome resistance. Cancer Cell 39, 151–153.
Targeting the microbiome to overcome resistance.Crossref | GoogleScholarGoogle Scholar | 33561397PubMed |

[36]  Batten, M. et al. (2020) Gut microbiota predicts response and toxicity with neoadjuvant immunotherapy. Cancer Res. 80, 5734.

[37]  Kovatcheva-Datchary, P. et al. (2015) Dietary fiber-induced improvement in glucose metabolism is associated with increased abundance of Prevotella. Cell Metab. 22, 971–982.
Dietary fiber-induced improvement in glucose metabolism is associated with increased abundance of Prevotella.Crossref | GoogleScholarGoogle Scholar | 26552345PubMed |

[38]  Healey, G. et al. (2016) Influence of habitual dietary fibre intake on the responsiveness of the gut microbiota to a prebiotic: protocol for a randomised, double-blind, placebo-controlled, cross-over, single-centre study. BMJ Open 6, e012504.
Influence of habitual dietary fibre intake on the responsiveness of the gut microbiota to a prebiotic: protocol for a randomised, double-blind, placebo-controlled, cross-over, single-centre study.Crossref | GoogleScholarGoogle Scholar | 27591024PubMed |

[39]  Patnode, M.L. et al. (2019) Interspecies competition impacts targeted manipulation of human gut bacteria by fiber-derived glycans. Cell 179, 59–73 e13.
Interspecies competition impacts targeted manipulation of human gut bacteria by fiber-derived glycans.Crossref | GoogleScholarGoogle Scholar | 31539500PubMed |

[40]  Walker, A.W. et al. (2011) Dominant and diet-responsive groups of bacteria within the human colonic microbiota. ISME J. 5, 220–230.
Dominant and diet-responsive groups of bacteria within the human colonic microbiota.Crossref | GoogleScholarGoogle Scholar | 20686513PubMed |

[41]  Baxter, N.T. et al. (2019) Dynamics of human gut microbiota and short-chain fatty acids in response to dietary interventions with three fermentable fibers. MBio 10, e02566-18.
Dynamics of human gut microbiota and short-chain fatty acids in response to dietary interventions with three fermentable fibers.Crossref | GoogleScholarGoogle Scholar | 30696735PubMed |


Biographies

Emma Todd is a research assistant and prospective PhD student with a passion for understanding the gut–brain axis, with a strong interest in the relationship between the microbiome and mental health disorders.

Rebecca Simpson is a PhD student at the University of Sydney. Her research focuses on how diet and intestinal microbes influence anti-tumour immune responses and the development of immune mediated toxicities during immunotherapy.

Reem Elnour is a PhD student at the University of Sydney and has a passion for cancer pathogenesis and microbiology. She is particularly interested in the intestinal epithelial barrier and the role it has in colorectal cancer development.

Miguel Castaneda is a third-year PhD student at the University of Sydney with a keen interest in cancer immunology and microbiology.

Erin Shanahan is a microbiologist and University of Sydney à Beckett Bowel Cancer Research Fellow, based in the School of Life and Environmental Sciences. Her research focuses on diet-microbiome interactions in gut health and cancer.



* These authors contributed equally.