A reduced mathematical model of the acute inflammatory response II. Capturing scenarios of repeated endotoxin administration

Day, Judy; Rubin, Jonathan E.; Vodovotz, Yoram; Chow, Carson C.; Reynolds, Angela; Clermont, Gilles

doi:10.1016/j.jtbi.2006.02.015

Cited by 150 publications

(157 citation statements)

References 52 publications

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“…The response of TNF-α (T ) is also very small, compared to the first response. The response of ACTH ( A) and cortisol (F) is not detectable for the second injection.The results are similar to results found by Day et al (2006) and illustrate the significance of the system being in homeostasis, when exposed to LPS, such that tolerance is avoided. (1)- (2) presented in Sect.…”

Section: Repeated Lps Exposuresupporting

confidence: 86%

Integrated Inflammatory Stress (ITIS) Model

et al. 2017

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Integrated Inflammatory Stress (ITIS) ModelBangsgaard, Elisabeth O.; Hjorth, Poul G.; Olufsen, Mette S.; Mehlsen, Jesper; Ottesen, Johnny T. Published in: Bulletin of Mathematical BiologyLink to article, DOI: 10.1007/s11538-017-0293-2 Publication date: 2017 Document VersionPublisher's PDF, also known as Version of record Abstract During the last decade, there has been an increasing interest in the coupling between the acute inflammatory response and the Hypothalamic-Pituitary-Adrenal (HPA) axis. The inflammatory response is activated acutely by pathogen-or damagerelated molecular patterns, whereas the HPA axis maintains a long-term level of the stress hormone cortisol which is also anti-inflammatory. A new integrated model of the interaction between these two subsystems of the inflammatory system is proposed and coined the integrated inflammatory stress (ITIS) model. The coupling mechanisms describing the interactions between the subsystems in the ITIS model are formulated based on biological reasoning and its ability to describe clinical data. The ITIS model is calibrated and validated by simulating various scenarios related to endotoxin (LPS) exposure. The model is capable of reproducing human data of tumor necrosis factor alpha, adrenocorticotropic hormone (ACTH) and cortisol and suggests that repeated LPS injections lead to a deficient response. The ITIS model predicts that the most extensive response to an LPS injection in ACTH and cortisol concentrations is observed in the early hours of the day. A constant activation results in elevated levels of the variables in the model while a prolonged change of the oscillations in ACTH and

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Section: Repeated Lps Exposuresupporting

confidence: 86%

Integrated Inflammatory Stress (ITIS) Model

et al. 2017

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“…The majority of the parameter values for this model are taken directly from two previous models of the inflammatory response [9,23]. The remaining unknown parameters are approximated according to experimental observations and biological assumptions.…”

Section: Methodsmentioning

confidence: 99%

“…Building upon insights established by theoretical models of the acute inflammatory response [9,[23][24][25][26], the current study aims to analyze the impact of pathologic bacteria in the context of NEC, as motivated by Hunter et al [27], and to predict the conditions under which probiotics may be successful in promoting the health and survival of infants at risk for NEC. Pathogenic and probiotic bacteria populations initially present in the intestinal lumen are simulated using an ordinary differential equation model.…”

Section: Current Modelmentioning

confidence: 99%

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

Arciero

Ermentrout

Rubin

et al. 2009

Journal of Critical Care

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Background: Necrotizing enterocolitis (NEC) is a severe disease of the gastrointestinal tract of pre-term babies and is thought to be related to the physiological immaturity of the intestine and altered levels of normal flora in the gut. Understanding the factors that contribute to the pathology of NEC may lead to the development of treatment strategies aimed at re-establishing the integrity of the epithelial wall and preventing the propagation of inflammation in NEC. Several studies have shown a reduced incidence and severity of NEC in neonates treated with probiotics (beneficial bacteria species).

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“…This type of modeling has been successful in yielding basic insights into acute inflammation [75][76][77][78] including quantitative insights into the biology underlying experimental paradigms of acute inflammation in animals [79][80][81]. A more recent concept has been that of "Translational Systems Biology" [11,72,82,108], which includes computational simulations of clinical trials [83][84][85][86], potential clinical diagnostics in the form of patientspecific models [144], streamlined usage of experimental animals [87], and rational device design [89].…”

Section: Systems Biology Approaches Can Shed Insight Into Inflammatiomentioning

confidence: 99%

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

Namas¹,

Ghuma²,

Hermus

et al. 2008

Libyan Journal of Medicine

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Abstract; Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.

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A reduced mathematical model of the acute inflammatory response II. Capturing scenarios of repeated endotoxin administration

Cited by 150 publications

References 52 publications

Integrated Inflammatory Stress (ITIS) Model

Integrated Inflammatory Stress (ITIS) Model

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

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

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