Quantifying Information Exchange Between Cells in Inflammaging

Open

Israr B. M. Ibrahim, Ramana M. Pidaparti

2026 Bioengineering Vol. 13 Issue 2 Article Cited by 0 SDG 17SDG 3 Quartile

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. © 2026 by the authors.

Affiliations

Department of Mechanical and Industrial Engineering, Universitas Syiah Kuala, Banda Aceh, 23111, Indonesia; College of Engineering, University of Georgia, Athens, 30602, GA, United States

Research at a Glance

Premium content — register to unlock

Research at a Glance

Register to unlock

Topics & SDG Alignment

Premium content — register to unlock

Topics & SDG Alignment

Register to unlock

Collaboration

Premium content — register to unlock

Collaboration

Register to unlock

Author Profile (Selected)

Premium content — register to unlock

Author Profile (Selected)

Register to unlock

References Overview

Premium content — register to unlock

References Overview

Register to unlock

Journal & Source

Premium content — register to unlock

Journal & Source

Register to unlock

Metadata & Integrity

Premium content — register to unlock

Metadata & Integrity

Register to unlock