Cross-kingdom sensing: investigating platelet-released signals and bacterial responding mechanisms in bacterial lifestyles switch and biofilm formation

Maintaining health balance between hosts and commensal microorganisms fulfils microbial nutritional demand and also benefits to hosts for gaining unique metabolites and “training” in host immune systems against other virulent invaders. However, occasionally, commensal bacteria detach from their original niche (e.g. skin surface or oral cavity) and enter exclusive locations (e.g. bloodstream or deeper layers of skin), which could induce their pathogenicity and cause infections. Commensal Streptococci and Staphylococci from human skin or oral cavity can cross into the bloodstream through daily tooth brushing, invasive treatments, or wounds. To survive from immune attacks in blood stream, forming aggregation or biofilm on tissue surfaces can provide shield and protection. Compared to their planktonic counterparts, bacteria embedded within biofilms show greater resistance to external challenges due to self-produced and well-organized extracellular polymeric substances, which are constantly shaped by constituent bacteria and surrounding host cells. Previous studies have suggested that forming a platelet thrombus on minor endothelial lesions can attract planktonic bacterial attachment to promote further damage, platelet aggregation, and bacterial attachment. This vicious circle will result in complex bacteria-platelet biofilm and cause severe inflammation and tissue damages such as infective endocarditis. Bacterial surface proteins or compounds have been shown to induce the activation and aggregation of platelets. Nevertheless, whether diffusible molecules released by activated platelets can interact with bacterial sensing/regulating systems and induce the regulatory switch from bacterial planktonic lifestyle toward sessile status for biofilm formation is unclear.

Bacteria, through diffusible signal molecules, can communicate within their own population and express a particular phenotype in a collective manner in response to environmental stimuli. These molecule-based communications are not limited within the bacterial community but can extend to receive and interact with host cell signalling. We hypothesise that the formation of bacteria-platelet biofilms is initiated by complex bi-direction communications between bacteria and platelets. This project aims to investigate platelet signal molecules and bacterial sensing/regulating pathways involved in biofilm formation by molecular microbiology and transcriptomics approaches. This project is to bring a multidisciplinary team of scientists for advancing our understanding in bacteria-host interactions and is expected to pave a path for developing novel strategies to maintain health balance with our commensal microbiota. The student will have the opportunity to spend time in supervisors’ laboratories in Newcastle and Liverpool for gaining outstanding training in a wide range of state-of-the-art technologies.

Informal enquiries may be made to chienyi.chang@newcastle.ac.uk

HOW TO APPLY 

Applications should be made by emailing bbsrcdtp@liverpool.ac.uk with a CV and a covering letter, including whatever additional information you feel is pertinent to your application; you may wish to indicate, for example, why you are particularly interested in the selected project/s and at the selected University. Applications not meeting these criteria will be rejected. We will also require electronic copies of your degree certificates and transcripts.

In addition to the CV and covering letter, please email a completed copy of the Newcastle-Liverpool-Durham (NLD) BBSRC DTP Studentship Application Details Form (Word document) to bbsrcdtp@liverpool.ac.uk, noting the additional details that are required for your application which are listed in this form. A blank copy of this form can be found at: https://www.nld-dtp.org.uk/how-apply.