# Quantifying Information Exchange Between Cells in Inflammaging

## TL;DR

This study uses a computer model to show how aging disrupts communication between immune and skin cells during inflammation, leading to slower healing.

## Contribution

The paper introduces a novel computational model to quantify and visualize cell communication dynamics during inflammaging.

## Key findings

- Inflammaging reduces cell–cell information exchange and increases cellular noise compared to normal inflammation.
- Normal inflammation shows higher fibroblast centrality, while inflammaging shows increased macrophage centrality in communication networks.
- Network topology reflects the primary cell types driving inflammation and its progression.

## Abstract

Inflammaging is inflammation caused by altered cell–cell communications due to aging which leads to impaired wound healing. In this study, we investigated the underlying dynamics of information exchange between macrophage and fibroblast cells during inflammation using an in silico agent-based model. Information exchange was inferred through migration dynamics of motile cells, and network representations of cell–cell information exchange were built. We investigated information exchange through computational modelling during inflammation with two different courses: inflammation followed by full recovery, and inflammation followed by sustained injury due to aging progression. We found that inflammaging leads to reduced cell–cell information exchange and noisier dynamics of cells compared to normal inflammation. Normal inflammation favours higher centrality on the fibroblast nodes, while inflammaging prefers networks with more centrality on the macrophage nodes. This network topology may indicate the primary agents in the inflammation and provide a way to describe inflammation and its course by a network of cell–cell interactions.