Dr Amanda Eve Rossiter BSc PhD

Amanda Rossiter

Institute of Microbiology and Infection
Lecturer in Prokaryotic Infection Biology

Contact details

Institute of Microbiology and Infection
Tower 101, Biosciences
University of Birmingham
B15 2TT

Dr Rossiter's research focuses on bacterial pathogenesis, with a particular interest in Salmonella spp. and Helicobacter pylori infections. Dr Rossiter is investigating how H. pylori-mediated modulation of the hosts immune system and gastrointestinal microbiome can lead to the development of gastric cancer or, on the contrary, protect against auto-immune disorders, such as Inflammatory Bowel Disease. 


  • PhD Microbiology (University of Birmingham)
  • BSc Biochemistry (University of Liverpool)


Amanda received her PhD from the University of Birmingham, where she took a particular interest in the biogenesis of secreted virulence determinants from Gram-negative pathogens. Her early post-doctoral work focused on the applications of these bacterial secretion systems as a platform for vaccine delivery, using attenuated Salmonella strains.

Amanda was awarded a 4-year Sir Henry Wellcome Fellowship in 2013, to study immunosuppressive bacterial antigens. During the first year of the fellowship, Amanda undertook a research visit to Monash University, in Melbourne to work with a murine model of Helicobacter pylori infection; the bacterium that is the leading cause of gastric cancer.

She has since returned to the University of Birmingham to establish an independent research group focusing on how H. pylori modulates the host immune system and gastrointestinal microbiome in the development of gastric cancer. 


Postgraduate supervision

Amanda is enthusiastic about speaking with students that have a passion for research and who would like to join the lab to study an MSc or PhD.

If you are interested in joining the group, please contact Amanda directly.


The Rossiter lab focuses on the bacterium H. pylori and its dichotomic association with Inflammatory Bowel Disease (IBD) and gastric cancer. Epidemiology suggests that gastric H. pylori infection can protect against IBD, yet H. pylori is most famous for being the biggest risk factor for gastric cancer. Amanda’s lab uses a combination of human clinical samples, mouse models and in vitro systems to investigate the mechanisms underpinning these fascinating relationships between H. pylori and its human host, with a specific focus on the manipulation of the host immune system and gastrointestinal microbiome by H. pylori.

Helicobacter pylori; an enigmatic bacterial pathogen

Helicobacter pylori has a unique evolutionary relationship with its human host, as it has colonised the stomach since the migration of modern humans out of Africa over 60,000 years ago. It is one of the most prevalent bacterial infections, present in nearly 50% of people worldwide. Most people will remain asymptomatic, however, a very small subset of infections (1%) develop gastric cancer. Intriguingly, those infected with H. pylori have a lower risk of developing auto-immune disorders, such as Inflammatory Bowel Disease (IBD). The reasons for the huge variation in clinical outcomes associated with H. pylori infections, or indeed its apparent protection against IBD, are not clearly understood.

H. pylori and the gastrointestinal microbiome

Amanda’s current research focuses on the role of the gastric pathogen H. pylori on shaping the gastrointestinal microbiome, in health and disease. When H. pylori infects the human stomach, it is able to dominate the gastric microbiome to represent nearly 95% of the microbial community. However, distinct changes occur in the gastric microbiome during the progression to gastric cancer, whereby the abundance of H. pylori significantly decreases and the microbial diversity is enriched with bacteria that are thought to be opportunistic commensals from the intestine. Thus, understanding what causes these drastic changes in the landscape of the gastric microbiome is hugely important in understanding gastric carcinogenesis.

To study this, Amanda’s research focuses on how H. pylori brings about changes to the gastrointestinal microbiome and T-cell mediated inflammation in patients suffering with gastric cancer and IBD, working closely with gastroenterologists at the Queen Elizabeth Hospital. Mouse models of H. pylori infection and colitis are used to explore the mechanisms underlying how H. pylori can harm, or help, its host. Amanda also has an interest in pathogenic mechanisms employed by Gram-negative pathogens and as such, uses mouse models of Salmonella Typhimurium and H. pylori infection to study immunosuppressive virulence determinants that are conserved between pathogenic members of the Proteobacteria phylum.  

Other activities

  • Microbiology Society Champion
  • Member of the Advisory Board for the Publishing Committee of the Microbiology Society


Sevastsyanovich YR, Withers DR, Marriott CL, Morris FC, Wells TJ, Browning DF, Beriotto I, Ross E, Ali HO, Wardius CA, Cunningham AF, Henderson IR, Rossiter AE. 2017. Antigen Localization Influences the Magnitude and Kinetics of Endogenous Adaptive Immune Response to Recombinant Salmonella Vaccines. Infect Immun 85.

Hutton ML, D'Costa K, Rossiter AE, Wang L, Turner L, Steer DL, Masters SL, Croker BA, Kaparakis-Liaskos M, Ferrero RL. 2017. A Helicobacter pylori Homolog of Eukaryotic Flotillin Is Involved in Cholesterol Accumulation, Epithelial Cell Responses and Host Colonization. Frontiers in Cellular and Infection Microbiology 7.

Dunne KA, Chaudhuri RR, Rossiter AE, Beriotto I, Browning DF, Squire D, Cunningham AF, Cole JA, Loman N, Henderson IR. 2017. Sequencing a piece of history: complete genome sequence of the original Escherichia coli strain. Microbial Genomics 3.

Nichols KB, Totsika M, Moriel DG, Lo AW, Yang J, Wurpel DJ, et al. Molecular characterisation of the Vacuolating Autotransporter Toxin in Uropathogenic Escherichia coli. Journal of bacteriology. 2016.

Rossiter AE, Godfrey RE, Connolly JA, Busby SJ, Henderson IR, Browning DF. Expression of different bacterial cytotoxins is controlled by two global transcription factors, CRP and Fis, that co-operate in a shared-recruitment mechanism. The Biochemical journal. 2015;466(2):323-35.

Browning DF, Bavro VN, Mason JL, Sevastsyanovich YR, Rossiter AE, Jeeves M, et al. Cross-species chimeras reveal BamA POTRA and beta-barrel domains must be fine-tuned for efficient OMP insertion. Molecular microbiology. 2015;97(4):646-59.

Browning DF, Matthews SA, Rossiter AE, Sevastsyanovich YR, Jeeves M, Mason JL, et al. Mutational and topological analysis of the Escherichia coli BamA protein. PloS one. 2013;8(12):e84512.

Chintakayala K, Singh SS, Rossiter AE, Shahapure R, Dame RT, Grainger DC. E. coli Fis protein insulates the cbpA gene from uncontrolled transcription. PLoS genetics. 2013;9(1):e1003152.

Leyton DL, Rossiter AE, Henderson IR. From self sufficiency to dependence: mechanisms and factors important for autotransporter biogenesis. Nature reviews Microbiology. 2012;10(3):213-25.

Rossiter AE, Browning DF, Leyton DL, Johnson MD, Godfrey RE, Wardius CA, et al. Transcription of the plasmid-encoded toxin gene from enteroaggregative Escherichia coli is regulated by a novel co-activation mechanism involving CRP and Fis. Molecular microbiology. 2011;81(1):179-91.

Rossiter AE, Leyton DL, Tveen-Jensen K, Browning DF, Sevastsyanovich Y, Knowles TJ, et al. The essential beta-barrel assembly machinery complex components BamD and BamA are required for autotransporter biogenesis. Journal of bacteriology. 2011;193(16):4250-3.

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