Computational Modeling of Inflammation and Wound Healing

Ziraldo, Cordelia; Mi, Qi; An, Gary; Vodovotz, Yoram

doi:10.1089/wound.2012.0416

Cited by 36 publications

(28 citation statements)

References 50 publications

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“…CFD has also been used to analyze possible design optimization routes for grafts for both hemodialysis (Canneyt et al, 2013 ), coronary artery stents looking at the flow within stent struts (Gundert et al, 2012 ), comparing different stent geometries (Gogas et al, 2014 ) and the effect of deformable stents (Martin et al, 2014 ), peripheral bypasses (Grus et al, 2016 ), and novel grafting systems such as an endograft for aneurysm repair (Aristokleous et al, 2015 ) and a mechanism of external vein graft support (Meirson et al, 2015 ). Moreover, new studies looking at the interaction between mechanical forces and cell response for instance used agent based (Ziraldo et al, 2013 ), hybrid agent based-continuum (Garbey et al, 2015 ), coupled agent-based and finite element (Zahedmanesh and Lally, 2011 ), and mechanistic approaches (Goodman et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Patient-Specific, Multi-Scale Modeling of Neointimal Hyperplasia in Vein Grafts

et al. 2017

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Neointimal hyperplasia is amongst the major causes of failure of bypass grafts. The disease progression varies from patient to patient due to a range of different factors. In this paper, a mathematical model will be used to understand neointimal hyperplasia in individual patients, combining information from biological experiments and patient-specific data to analyze some aspects of the disease, particularly with regard to mechanical stimuli due to shear stresses on the vessel wall. By combining a biochemical model of cell growth and a patient-specific computational fluid dynamics analysis of blood flow in the lumen, remodeling of the blood vessel is studied by means of a novel computational framework. The framework was used to analyze two vein graft bypasses from one patient: a femoro-popliteal and a femoro-distal bypass. The remodeling of the vessel wall and analysis of the flow for each case was then compared to clinical data and discussed as a potential tool for a better understanding of the disease. Simulation results from this first computational approach showed an overall agreement on the locations of hyperplasia in these patients and demonstrated the potential of using new integrative modeling tools to understand disease progression.

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Section: Discussionmentioning

confidence: 99%

Patient-Specific, Multi-Scale Modeling of Neointimal Hyperplasia in Vein Grafts

et al. 2017

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“…The model of Penner et al (2012) describes spatial interactions of a generic group of inflammatory cells, chemokines and anti-inflammatory cytokines, and exhibits interesting spatial patterns such as travelling waves, localised breathers and spatially inhomogeneous temporal oscillations. Recent advances in technology are leading to an increase in experimental data that highlight the spatial interactions underpinning inflammatory processes and mechanistic mathematical models alongside the computational techniques necessary to analyse such complex datasets are being used to interpret and elucidate the spatial interactions seen in the data (Liepe et al 2012;Ziraldo et al 2013;Weavers et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms and Points of Control in the Spread of Inflammation: A Mathematical Investigation

et al. 2020

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Understanding the mechanisms that control the body's response to inflammation is of key importance, due to its involvement in myriad medical conditions, including cancer, arthritis, Alzheimer's disease and asthma. While resolving inflammation has historically been considered a passive process, since the turn of the century the hunt for novel therapeutic interventions has begun to focus upon active manipulation of constituent mechanisms, particularly involving the roles of apoptosing neutrophils, phagocytosing macrophages and anti-inflammatory mediators. Moreover, there is growing interest in how inflammatory damage can spread spatially due to the motility of inflammatory mediators and immune cells. For example, impaired neutrophil chemotaxis is implicated in causing chronic inflammation under trauma and in ageing, while neutrophil migration is an attractive therapeutic target in ailments such as chronic obstructive pulmonary disease. We extend an existing homogeneous model that captures interactions between inflammatory mediators, neutrophils and macrophages to incorporate spatial behaviour. Through bifurcation analysis and numerical simulation, we show that spatially inhomogeneous outcomes can present close to the switch from bistability to guaranteed resolution in the corresponding homogeneous model. Finally, we show how aberrant spatial mechanisms can play a role in the failure of inflammation to resolve and discuss our results within the broader context of seeking novel inflammatory treatments.

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“…We analyzed wound tissue chemokine and cytokine levels in MRSA-infected mice at 1, 3, and 5 days after treatment. Inflammatory mediators, such as tumor necrosis factor alpha (TNF-α), interferon-γ, interleukin (IL)-6, IL-10, transforming growth factor beta-1 (TGF-β1), and nitric oxide, modulate the wound-healing response [ 21 ]. MRSA-infected mice were used as a positive control to confirm cytokine activation.…”

Section: Resultsmentioning

confidence: 99%

Use of tilapia piscidin 3 (TP3) to protect against MRSA infection in mice with skin injuries

et al. 2015

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Antimicrobial peptides (AMPs), represent promising agents for new therapeutic approaches of infected wound treatment, on account of their antimicrobial and wound closure activities, and low potential for inducing resistance. However, therapeutic applications of these AMPs are limited by their toxicity and low stability in vivo. Previously, we reported that the 23 amino-acid designer peptide TP3 possessed antimicrobial activities. Here, we analyzed the wound closure activities of TP3 both and in vivo. TP3 at doses of up to 40 μg/ml did not affect the viability of baby hamster kidney cells. Furthermore, TP3 was found to be highly effective at combating peritonitis and wound infection caused by MRSA in mouse models, without inducing adverse behavioral effects or liver or kidney toxicity. TP3 treatment increased survival by 100% at 8 days after infection, and accelerated the progression of proliferation, remodeling, and maturation of infected wounds. Taken together, our results indicate that TP3 enhances the rate of survival of mice infected with the bacterial pathogen MRSA through both antimicrobial and immunomodulatory effects. Overall, these results suggest that TP3 may be suitable for development as a novel topical agent for treatment of infected wounds.

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Computational Modeling of Inflammation and Wound Healing

Cited by 36 publications

References 50 publications

Patient-Specific, Multi-Scale Modeling of Neointimal Hyperplasia in Vein Grafts

Patient-Specific, Multi-Scale Modeling of Neointimal Hyperplasia in Vein Grafts

Mechanisms and Points of Control in the Spread of Inflammation: A Mathematical Investigation

Use of tilapia piscidin 3 (TP3) to protect against MRSA infection in mice with skin injuries

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