Jai graduated from the University of Surrey in 2011 and enjoyed it enough to return to complete his MSc in Medical Microbiology (Research) [2012-2013] and PhD in Microbiology .
After a brief spell as a Post-Doctoral Research Assistant at the University of Reading [2016-2017], Jai returned to Surrey yet again where he currently works as a Research Fellow in Molecular Microbiology in the new School of Veterinary Medicine.
Areas of specialism
University roles and responsibilities
- ECR Representative for Vet School
Jai is a member of the La Ragione Bacteriology Group whose research is focused on understanding the detailed mechanisms that bacterial pathogens of veterinary and medical importance employ in order to colonise the host. Through a greater understanding of the pathobiology of these economically important pathogens the group hopes to develop novel intervention strategies. Jai’s particular interest is in Host/Pathogen interactions of zoonotic agents such as Campylobacter and E. coli with an emphasis on vaccine development for use in livestock.
Campylobacter is a common cause of diarrhoeal illness in the developed world, with EFSA estimating an annual incidence of up to 20 million cases of campylobacteriosis in the EU. Jai’s PhD research identified and characterised novel virulence factors in Campylobacter jejuni and Campylobacter coli, thereby providing insights into disease causing mechanisms of these enigmatic pathogens.
Currently, Jai’s research is centred on a collaborative project with the University of Reading and industrial partners aiming to combat avian colibacillosis, a range of syndromes in poultry caused the bacteria Escherichia coli. Colibacillosis is a common disease that is seen worldwide and is of significant economic importance concerning the loss of livestock. Jai’s aim is to develop novel vaccines against avian pathogenic E. coli (APEC) using a combination of genomic and molecular biology approaches.
Jai also has a strong interest in using synthetic biology and molecular biology techniques in order to engineer improved vaccines, probiotics and other alternatives to antibiotics.
The capC gene was initially confirmed as being encoded by approximately 60% of C. jejuni and C. coli human clinical and poultry associated isolates. Moreover, CapC was confirmed as a member of the autotransporter family through the use of bioinformatic prediction tools and the localisation site of this protein was determined as the outer membrane of C. jejuni. Targeted mutagenesis of the capC gene in C. jejuni 81116 and C. jejuni M1 and subsequent comparison of wild-type and isogenic mutant strains demonstrated that CapC contributes directly to virulence in the Galleria mellonella invertebrate model (p=0.00017; p=0.002323). Furthermore, tissue culture assays using non-polarised, partially differentiated Caco-2 and T84 intestinal epithelial cells indicate that deletion of CapC resulted in significantly decreased adhesion and invasion efficiency. Additional analyses indicated that CapC primarily contributes to adhesion to intestinal epithelial cells. Additional assays showed that deletion of the capC gene has no significant phenotypic effect on cytotoxicity in a Caco-2 cell model.
A secondary aim of this study was to examine the distribution of capC amongst campylobacters and to establish any potential genetic associations of this virulence determinant. Using publically
available genome sequences, capC was established to be highly prevalent in C. jejuni (67.9%) and C. coli (84%). Campylobacter autotransporter proteins were also shown to be present in truncated and full length forms. Interestingly, full length CapC was shown to be primarily associated with the ST-45, ST-283 and ST-573 clonal complexes in C. jejuni and the ST-828 clonal complex in C. coli. Furthermore, this study detailed the identification of a novel autotransporter in Campylobacter species, tentatively designated as CapD. This autotransporter was found to be genetically distinct from CapC and is the most prevalent autotransporter identified in Campylobacter species.
The studies presented in this thesis indicate that CapC is a strain-specific virulence determinant in Campylobacter species that is associated with select lineages of C. jejuni and C. coli. CapC contributes to the integral infection process of adhesion however further studies are required to fully elucidate the exact nature of this interaction. Additionally, it can be concluded that possession of Campylobacter autotransporter proteins is dependent on genetic background.