Coupled Immunological and Biomechanical Model of Emphysema Progression

Authored by Mario Ceresa, Andy L Olivares, Jerome Noailly, Ballester Miguel A Gonzalez

Date Published: 2018

DOI: 10.3389/fphys.2018.00388

Sponsors: Spanish Ministry of Science and Innovation (MICINN)

Platforms: No platforms listed

Model Documentation: Other Narrative Flow charts

Model Code URLs: Model code not found

Abstract

Chronic Obstructive Pulmonary Disease (COPD) is a disabling respiratory pathology, with a high prevalence and a significant economic and social cost. It is characterized by different clinical phenotypes with different risk profiles. Detecting the correct phenotype, especially for the emphysema subtype, and predicting the risk of major exacerbations are key elements in order to deliver more effective treatments. However, emphysema onset and progression are influenced by a complex interaction between the immune system and the mechanical properties of biological tissue. The former causes chronic inflammation and tissue remodeling. The latter influences the effective resistance or appropriate mechanical response of the lung tissue to repeated breathing cycles. In this work we present a multi-scale model of both aspects, coupling Finite Element (FE) and Agent Based (AB) techniques that we would like to use to predict the onset and progression of emphysema in patients. The AB part is based on existing biological models of inflammation and immunological response as a set of coupled non-linear differential equations. The FE part simulates the biomechanical effects of repeated strain on the biological tissue. We devise a strategy to couple the discrete biological model at the molecular /cellular level and the biomechanical finite element simulations at the tissue level. We tested our implementation on a public emphysema image database and found that it can indeed simulate the evolution of clinical image biomarkers during disease progression.

Tags

Multiscale modeling Mechanisms Lung Agent-based models In-vivo Mechanical-properties Cardiac myocytes Tumor-necrosis-factor Factor-alpha Double-blind Emphysema Copd Chronic bronchitis Finite element methods Biophysical modeling Supercomputing Obstructive pulmonary-disease Macrophage activation Computed-tomography Cardiac myocytes Severe asthma Human lung Beta