Professor in Reproductive Immunobiology
I qualified as a veterinary surgeon (BVSc, MRCVS) in 1984 and worked in clinical practice for 14 years in Wales. Whilst in practice I studied for two clinical Diplomas (DBR, DCHP), and then started work on a PhD supervised by Prof Hilary Dobson at the University of Liverpool. In 1998 I moved to the Royal Veterinary College in London, and I was awarded my PhD by Liverpool University in 2002. In 2006 I was awarded a BBSRC Research Development Fellowship to further my interests in host-pathogen interactions.
In 2008 I was appointed to a Personal Chair in Reproductive Immunobiology at Swansea University Medical School. In 2013, I was awarded FRCVS for meritorious contributions to research, and in 2015 I was awarded the Schofield Prize.
For further details consult Wikipedia: https://en.wikipedia.org/wiki/Martin_Sheldon
My group study the mechanisms of interactions between hosts and pathogens. We are interested in how bacteria cause disease. On the other hand, we also aim to understand how animals and humans defend themselves against infections and prevent disease by avoiding, tolerating and resisting pathogenic bacteria.
Our first research question was what protects oocytes in the ovary from damage caused by these bacterial infections? I discovered that the function of the ovary is perturbed in animals with uterine bacterial infections. We initially worked on how microbes cause inflammation and tissue damage in the endometrium of the uterus, and how this affects the ovary and the oocyte. Key discoveries were that the epithelial and stromal cells of the endometrium, and the granulosa cells of the ovary have roles in innate immunity. In particular these cells express receptors, such as Toll-like Receptors (TLRs), which detect pathogen-associated molecular patterns to induce inflammatory responses, including the production of cytokines, chemokines and prostaglandins. Furthermore, we discovered that pathogen-associated molecules perturb oocyte health and development, linking bacterial infections to long-term impacts on fertility.
Our second research question is how do cells protect themselves against pore-forming toxins? Pore-forming toxins are the most common virulence factor used by bacteria to damage host cells, which leads to tissue pathology. We have focussed on cholesterol-dependent cytolysins, as these are the most common pore-forming toxin. We study the cellular responses to pore-forming toxins, and the molecular mechanisms of cytoprotection against pore-forming toxins in tissue cells. Increasing the protection of cells against bacterial virulence factors is an alternative to using antimicrobials to kill bacteria, helping in the fight against antimicrobial resistance.