Pawel is a theoretician by training (M.S in Control Theory, 2001, PhD in Statistics, 2006, PDRA in Centre for Cell Imaging, Liverpool, 2006-11), but for several years he has been using experimental approaches to investigate the regulation of inflammatory signalling networks. He is currently a Senior Lecturer in the Faculty of Biology, Medicine and Health where he established an experimental systems immunology lab (during his BBSRC David Phillips Fellowship, 2011-2016). He has developed quantitative live-cell imaging and gene expression platforms to study immune cell signalling, incorporating measurements of TF dynamics and transcription. Recently, he has developed protocols for quantitative single-cell approaches to study host-pathogen interactions of the Listeria monocytogenes, an important bacterial pathogen of man. 

Biological systems are inherently complex and exhibit unexpected dynamics. This complexity is associated with different levels of cellular organization, as genes, signaling networks and cells have to be simultaneously regulated in the tissue. A more quantitative understanding of these complex processes is key to understand and treat out-of-control responses associated with infections as well as many autoimmune and inflammatory diseases. My specific aim is to understand how a set of cellular and molecular cytokine networks controls the propagation and resolution of inflammatory signaling in time and space and how they contribute to outcomes of single-cell host-pathogen interactions. In order to achieve this new quantitative picture, we employ systems biology approaches that combine mathematics, live-cell microscopy, and immunology.

Single cell biology approach for immune cell signalling

Biological signalling systems are inherently complex and their regulation needs to be understood at all levels. One example is the failure to resolve inflammation in single cells, which is associated with out-of-control tissue-level responses characteristic in many autoimmune diseases.

My previous work has suggested that inflammation may be controlled through subtle changes in single cell dynamics and varying cellular heterogeneity through underlying molecular networks. We use an interdisciplinary systems biology approach to build a quantitative understanding of a set of cellular and molecular cytokine networks that together regulate inflammatory processes. We employ state-of-the-art multi-scale mathematical modelling, live-cell microscopy (including microfluidic tissue models) and quantitative single cell gene expression. Thses allow studies of emergence and function of spatial and temporal dynamics during inflammation. A more quantitative understanding of these non-linear and non-intuitive processes might lead to improved therapeutic strategies for inflammatory disease.