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.
Highlights
Chronic obstructive pulmonary disease (COPD) is estimated to affect more than 500 million people worldwide, causing significant disability, loss of quality of life and social burden, with costs in excess of e 56 billion per year in the European Union (Decramer et al, 2012)
We extended our previous work Ceresa et al (2017) to couple the dynamics of the biological events captured through agent cooperation in an agent-based (AB) model with a biomechanical simulation of the tissue captured by a coupled Finite Element (FE) Model that iteratively predicts the evolution of the mechanical cues transmitted to the cells inside the lungs
We modeled the simplified behavior of immune system cells such as alveolar macrophages and neutrophils, and cells in charge of wound healing mechanisms such as fibroblasts
Summary
Chronic obstructive pulmonary disease (COPD) is estimated to affect more than 500 million people worldwide, causing significant disability, loss of quality of life and social burden, with costs in excess of e 56 billion per year in the European Union (Decramer et al, 2012). The disease has a lifetime prevalence of about 28% and cigarette smoking is commonly considered to be the principal risk factor (Gershon et al, 2011). Recent projections suggest that COPD will be the third cause of global mortality by the year 2030. The pathogenesis of COPD is still not completely understood (Larsson, 2007; Yoshida and Tuder, 2007) and involves a number of multi-scale cellular processes, including airways inflammation, adaptation and innate immunity to cigarette smoking, sensitivity to self and not-self. Clinical management of COPD involves consistent use of inhaled corticosteroids that help reducing COPD mortality. Their efficacy is limited (Faner and Agustí, 2016) and many patients experience exacerbations and poor symptoms control (Brightling et al, 2012)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
