CANCELLED A Joint Seminar for Biomedical Sciences and Mathematical Sciences

Mathematical models of the inflammatory response

Atomic structure of a biological molecule
Seminars

As part of the School of Science and Technology Biomedical Sciences and Mathematical Sciences Research Seminar Series, Anahita Bayani, NTU presents: Mathematical models of the inflammatory response.

  • From: Wednesday 1 May 2019, 1.10 pm
  • To: Wednesday 1 May 2019, 2 pm
  • Location: 282, Erasmus Darwin, Nottingham Trent University, Clifton Campus, Clifton Lane, Nottingham, NG11 8NS

Past event

Event details

As part of the School of Science and Technology Biomedical Sciences and Mathematical Sciences Research Seminar Series, Anahita Bayani, NTU presents: Mathematical models of the inflammatory response.

Abstract

There is growing interest in inflammation due to its involvement in a myriad medical conditions. Recent investigations show that inflammation is actively controlled by anti-inflammatory processes that can be modulated therapeutically. Accordingly, the mechanisms that resolve inflammation are of great interest, the interactions between macrophages and neutrophil mediated pro-inflammatory processes in particular.


Existing mathematical models describing macrophage neutrophil interactions are limited by their design, which generally takes the approach of spatially averaging biological quantities across the affected tissue. Assuming spatial homogeneity becomes increasingly spurious as the spatial scale of the damage increases, with clusters of neutrophils causing significant local tissue damage, while inflammation may resolve elsewhere. Furthermore, recent evidence points to aspects of the inflammatory response being modied under ageing and trauma, with changes in e.g. directed neutrophil motility and the macrophage functional response potentially influencing long-term outcomes.


We deploy a series of models that describe the interactions between populations of macrophages, active and apoptotic neutrophils and groups of chemicals that act as pro and anti inflammatory mediators, focusing throughout upon spatially dependent facets of the inflammatory response. Via a hybrid approach, in which we combine a PDE-based description of mediators with an individual based cellular automata description of the cell populations, we examine how variation in key model parameters can affect the spatial homogeneity of the outcome.

In particular, we address the questions of whether initially localised damage can invade neighbouring healthy tissue, and the extent to which sub-optimal directed cell motility (such as that associated with ageing, or inflammatory conditions such as chronic obstructive pulmonary disease) can impact upon the long-term outcome.

We illustrate that changes to the values of physiologically relevant parameters can act as a switch between healthy and pathological scenarios; with careful parameters our approach exhibits scope for elucidating how these key mechanisms could be actively manipulated to potentially identify new therapeutic interventions.

Hosted by Dr David Chappell and Dr Martin Nelson

All welcome.

For any enquiries please contact Dr John Dickenson

Location details

Room/Building:

282, Erasmus Darwin

Address:

Nottingham Trent University
Clifton Campus
Clifton Lane
Nottingham
NG11 8NS

Past event

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