Mechanistic simulations of inflammation: Current state and future prospects

Abstract

Inflammation is a normal, robust physiological process. It can also be viewed as a complex system that senses and resolves homeostatic perturbations initiated from within the body (for example, in autoimmune disease) or from the outside (for example, in infections). Virtually all acute and chronic diseases are either driven or modulated by inflammation. The complex interplay between beneficial and harmful arms of the inflammatory response may underlie the lack of fully effective therapies for many diseases. Mathematical modeling is emerging as a frontline tool for understanding the complexity of the inflammatory response. A series of articles in this issue highlights various modeling approaches to inflammation in the larger context of health and disease, from intracellular signaling to whole-animal physiology. Here we discuss the state of this emerging field. We note several common features of inflammation models, as well as challenges and prospects for future studies.

Using a mathematical model to analyze the role of probiotics and inflammation in necrotizing enterocolitis

“…Pathogenic and probiotic bacteria populations initially present in the intestinal lumen are simulated using an ordinary differential equation model. The degree of intestinal wall permeability is a variable in the system that corresponds indirectly to the role that Damage-associated Molecular Pattern (DAMP) molecules play in propagating the positive feedback between inflammation and damage [28,29]. Based on this permeability, the conditions leading to bacterial translocation into the systemic circulation can be predicted.…”

“…In this way, we hope to improve clinical translation, as part of our larger Translational Systems Biology framework [29,[36][37][38][39]. In particular, we have included mathematical terms in our model that represent important effects that have been implicated in the development of NEC and some of the mechanisms through which probiotics are thought to act to effect its progression [1,14].…”

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

“…As in most cases of therapeutic immunomodulation, inhibition of MIP-1α is a two-edged sword, in this case an increased risk of late infection [49]. [114] system that is turned on during infection as well as tissue injury, including T/HS [92] and perhaps also TBI [115] (Fig. 3).…”

Gelam and Nenas Honeys Inhibit Proliferation of HT 29 Colon Cancer Cells by Inducing DNA Damage and Apoptosis while Suppressing Inflammation

“…Loss of regulation in apoptosis will cause uncontrollable cancer cells proliferation and therefore compounds that activate apoptosis are targeted to be a novel chemoprevention therapy for cancer (Sun et al, 2004). Inflammation is an immunological and patho-physiological response of tissues to infectious organisms, cancer, autoimmune disease, toxic chemical substances or physical injury (Vodovotz et al, 2009). There are many mediators of inflammation such as cytokines, nitric oxide (NO) and prostaglandin (PG).…”