An agent-based model of cellular dynamics and circadian variability in human endotoxemia
As cellular variability and circadian rhythmicity play critical roles in immune and inflammatory responses, we present in this study an agent-based model of human endotoxemia to examine the interplay between circadian controls, cellular variability and stochastic dynamics of inflammatory cytokines....
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| Veröffentlicht in: | PloS one 2013-01, Vol.8 (1), p.e55550 |
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| creator | Nguyen, Tung T Calvano, Steve E Lowry, Stephen F Androulakis, Ioannis P |
| description | As cellular variability and circadian rhythmicity play critical roles in immune and inflammatory responses, we present in this study an agent-based model of human endotoxemia to examine the interplay between circadian controls, cellular variability and stochastic dynamics of inflammatory cytokines. The model is qualitatively validated by its ability to reproduce circadian dynamics of inflammatory mediators and critical inflammatory responses after endotoxin administration in vivo. Novel computational concepts are proposed to characterize the cellular variability and synchronization of inflammatory cytokines in a population of heterogeneous leukocytes. Our results suggest that there is a decrease in cell-to-cell variability of inflammatory cytokines while their synchronization is increased after endotoxin challenge. Model parameters that are responsible for IκB production stimulated by NFκB activation and for the production of anti-inflammatory cytokines have large impacts on system behaviors. Additionally, examining time-dependent systemic responses revealed that the system is least vulnerable to endotoxin in the early morning and most vulnerable around midnight. Although much remains to be explored, proposed computational concepts and the model we have pioneered will provide important insights for future investigations and extensions, especially for single-cell studies to discover how cellular variability contributes to clinical implications. |
| doi_str_mv | 10.1371/journal.pone.0055550 |
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The model is qualitatively validated by its ability to reproduce circadian dynamics of inflammatory mediators and critical inflammatory responses after endotoxin administration in vivo. Novel computational concepts are proposed to characterize the cellular variability and synchronization of inflammatory cytokines in a population of heterogeneous leukocytes. Our results suggest that there is a decrease in cell-to-cell variability of inflammatory cytokines while their synchronization is increased after endotoxin challenge. Model parameters that are responsible for IκB production stimulated by NFκB activation and for the production of anti-inflammatory cytokines have large impacts on system behaviors. Additionally, examining time-dependent systemic responses revealed that the system is least vulnerable to endotoxin in the early morning and most vulnerable around midnight. Although much remains to be explored, proposed computational concepts and the model we have pioneered will provide important insights for future investigations and extensions, especially for single-cell studies to discover how cellular variability contributes to clinical implications.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0055550</identifier><identifier>PMID: 23383223</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Agent-based models ; Algorithms ; Analysis ; Biology ; Cell Survival - immunology ; Circadian Rhythm - immunology ; Circadian rhythms ; Computation ; Computer applications ; Computer Science ; Computer Simulation ; Cytokines ; Endotoxemia ; Endotoxemia - immunology ; Endotoxemia - metabolism ; Endotoxins ; Endotoxins - adverse effects ; Gene expression ; Humans ; Infections ; Inflammation ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation Mediators ; Leukocytes ; Models, Biological ; NF-κB protein ; Ordinary differential equations ; Physiology ; Proteins ; Rodents ; Signal transduction ; Stochasticity ; Studies ; Surgery ; Synchronism ; Synchronization ; Time Factors ; Variability ; Viral infections</subject><ispartof>PloS one, 2013-01, Vol.8 (1), p.e55550</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Nguyen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Nguyen et al 2013 Nguyen et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-f1273d439d63d139413583aae296aa21a701cf0f63795e35d0eae553f4ae6eb03</citedby><cites>FETCH-LOGICAL-c692t-f1273d439d63d139413583aae296aa21a701cf0f63795e35d0eae553f4ae6eb03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3559552/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3559552/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53770,53772,79347,79348</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23383223$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Frangogiannis, Nikolaos</contributor><creatorcontrib>Nguyen, Tung T</creatorcontrib><creatorcontrib>Calvano, Steve E</creatorcontrib><creatorcontrib>Lowry, Stephen F</creatorcontrib><creatorcontrib>Androulakis, Ioannis P</creatorcontrib><title>An agent-based model of cellular dynamics and circadian variability in human endotoxemia</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>As cellular variability and circadian rhythmicity play critical roles in immune and inflammatory responses, we present in this study an agent-based model of human endotoxemia to examine the interplay between circadian controls, cellular variability and stochastic dynamics of inflammatory cytokines. 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The model is qualitatively validated by its ability to reproduce circadian dynamics of inflammatory mediators and critical inflammatory responses after endotoxin administration in vivo. Novel computational concepts are proposed to characterize the cellular variability and synchronization of inflammatory cytokines in a population of heterogeneous leukocytes. Our results suggest that there is a decrease in cell-to-cell variability of inflammatory cytokines while their synchronization is increased after endotoxin challenge. Model parameters that are responsible for IκB production stimulated by NFκB activation and for the production of anti-inflammatory cytokines have large impacts on system behaviors. Additionally, examining time-dependent systemic responses revealed that the system is least vulnerable to endotoxin in the early morning and most vulnerable around midnight. Although much remains to be explored, proposed computational concepts and the model we have pioneered will provide important insights for future investigations and extensions, especially for single-cell studies to discover how cellular variability contributes to clinical implications.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23383223</pmid><doi>10.1371/journal.pone.0055550</doi><tpages>e55550</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Agent-based models Algorithms Analysis Biology Cell Survival - immunology Circadian Rhythm - immunology Circadian rhythms Computation Computer applications Computer Science Computer Simulation Cytokines Endotoxemia Endotoxemia - immunology Endotoxemia - metabolism Endotoxins Endotoxins - adverse effects Gene expression Humans Infections Inflammation Inflammation - immunology Inflammation - metabolism Inflammation Mediators Leukocytes Models, Biological NF-κB protein Ordinary differential equations Physiology Proteins Rodents Signal transduction Stochasticity Studies Surgery Synchronism Synchronization Time Factors Variability Viral infections |
| title | An agent-based model of cellular dynamics and circadian variability in human endotoxemia |
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