Mathematical modeling of the circadian dynamics of the neuroendocrine-immune network in experimentally induced arthritis
The circadian dynamics of important neuroendocrine-immune mediators have been implicated in progression of rheumatoid arthritis pathophysiology, both clinically as well as in animal models. We present a mathematical model that describes the circadian interactions between mediators of the hypothalami...
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| Veröffentlicht in: | American journal of physiology: endocrinology and metabolism 2016-08, Vol.311 (2), p.E310-E324 |
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| container_title | American journal of physiology: endocrinology and metabolism |
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| creator | Rao, R DuBois, D Almon, R Jusko, W J Androulakis, I P |
| description | The circadian dynamics of important neuroendocrine-immune mediators have been implicated in progression of rheumatoid arthritis pathophysiology, both clinically as well as in animal models. We present a mathematical model that describes the circadian interactions between mediators of the hypothalamic-pituitary-adrenal (HPA) axis and the proinflammatory cytokines. Model predictions demonstrate that chronically elevated cytokine expression results in the development of adrenal insufficiency and circadian variability in paw edema. Notably, our model also predicts that an increase in mean secretion of corticosterone (CST) after the induction of the disease is accompanied by a decrease in the amplitude of the CST oscillation. Furthermore, alterations in the phase of circadian oscillation of both cytokines and HPA axis mediators are observed. Therefore, by incorporating the circadian interactions between the neuroendocrine-immune mediators, our model is able to simulate important features of rheumatoid arthritis pathophysiology. |
| doi_str_mv | 10.1152/ajpendo.00006.2016 |
| format | Article |
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We present a mathematical model that describes the circadian interactions between mediators of the hypothalamic-pituitary-adrenal (HPA) axis and the proinflammatory cytokines. Model predictions demonstrate that chronically elevated cytokine expression results in the development of adrenal insufficiency and circadian variability in paw edema. Notably, our model also predicts that an increase in mean secretion of corticosterone (CST) after the induction of the disease is accompanied by a decrease in the amplitude of the CST oscillation. Furthermore, alterations in the phase of circadian oscillation of both cytokines and HPA axis mediators are observed. Therefore, by incorporating the circadian interactions between the neuroendocrine-immune mediators, our model is able to simulate important features of rheumatoid arthritis pathophysiology.</description><identifier>ISSN: 0193-1849</identifier><identifier>EISSN: 1522-1555</identifier><identifier>DOI: 10.1152/ajpendo.00006.2016</identifier><identifier>PMID: 27221115</identifier><identifier>CODEN: AJPMD9</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Adrenocorticotropic Hormone - metabolism ; Animals ; Arthritis ; Arthritis, Experimental - immunology ; Arthritis, Experimental - metabolism ; Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - metabolism ; Circadian rhythm ; Circadian Rhythm - immunology ; Corticosterone - metabolism ; Corticotropin-Releasing Hormone - metabolism ; Cytokines ; Cytokines - immunology ; Endocrine system ; Experiments ; Hypothalamo-Hypophyseal System - metabolism ; Immune system ; Mathematical models ; Models, Theoretical ; Pituitary-Adrenal System - metabolism ; Receptors, Glucocorticoid - metabolism ; Rodentia</subject><ispartof>American journal of physiology: endocrinology and metabolism, 2016-08, Vol.311 (2), p.E310-E324</ispartof><rights>Copyright © 2016 the American Physiological Society.</rights><rights>Copyright American Physiological Society Aug 1, 2016</rights><rights>Copyright © 2016 the American Physiological Society 2016 American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-50d25b30690c7571de76b374533443dfaa61b837848215dba2bae0898f53af413</citedby><cites>FETCH-LOGICAL-c463t-50d25b30690c7571de76b374533443dfaa61b837848215dba2bae0898f53af413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27221115$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rao, R</creatorcontrib><creatorcontrib>DuBois, D</creatorcontrib><creatorcontrib>Almon, R</creatorcontrib><creatorcontrib>Jusko, W J</creatorcontrib><creatorcontrib>Androulakis, I P</creatorcontrib><title>Mathematical modeling of the circadian dynamics of the neuroendocrine-immune network in experimentally induced arthritis</title><title>American journal of physiology: endocrinology and metabolism</title><addtitle>Am J Physiol Endocrinol Metab</addtitle><description>The circadian dynamics of important neuroendocrine-immune mediators have been implicated in progression of rheumatoid arthritis pathophysiology, both clinically as well as in animal models. We present a mathematical model that describes the circadian interactions between mediators of the hypothalamic-pituitary-adrenal (HPA) axis and the proinflammatory cytokines. Model predictions demonstrate that chronically elevated cytokine expression results in the development of adrenal insufficiency and circadian variability in paw edema. Notably, our model also predicts that an increase in mean secretion of corticosterone (CST) after the induction of the disease is accompanied by a decrease in the amplitude of the CST oscillation. Furthermore, alterations in the phase of circadian oscillation of both cytokines and HPA axis mediators are observed. Therefore, by incorporating the circadian interactions between the neuroendocrine-immune mediators, our model is able to simulate important features of rheumatoid arthritis pathophysiology.</description><subject>Adrenocorticotropic Hormone - metabolism</subject><subject>Animals</subject><subject>Arthritis</subject><subject>Arthritis, Experimental - immunology</subject><subject>Arthritis, Experimental - metabolism</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - metabolism</subject><subject>Circadian rhythm</subject><subject>Circadian Rhythm - immunology</subject><subject>Corticosterone - metabolism</subject><subject>Corticotropin-Releasing Hormone - metabolism</subject><subject>Cytokines</subject><subject>Cytokines - immunology</subject><subject>Endocrine system</subject><subject>Experiments</subject><subject>Hypothalamo-Hypophyseal System - metabolism</subject><subject>Immune system</subject><subject>Mathematical models</subject><subject>Models, Theoretical</subject><subject>Pituitary-Adrenal System - metabolism</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>Rodentia</subject><issn>0193-1849</issn><issn>1522-1555</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUk1v1DAQtRCILgt_gAOKxKWXLP7MxwUJVRSQinppz9bEnnS9JPZiJ6X773HabQWc8MXSvDdv3tiPkLeMbhhT_APs9uht2NB8qg2nrHpGVhngJVNKPScrylpRska2J-RVSrtMq5XkL8kJrzlnWWNF7r7DtMURJmdgKMZgcXD-pgh9kcuFcdGAdeALe_AwOpMeEY9zDMt0E53H0o3j7Jfq9CvEH4XzBd7tMboR_QTDcMgVOxu0BcRpG93k0mvyooch4ZvjvSbX55-vzr6WF5dfvp19uiiNrMRUKmq56gStWmpqVTOLddWJWiohpBS2B6hY14i6kQ1nynbAO0DatE2vBPSSiTX5-KC7n7sRrcmGIgx6n71BPOgATv-NeLfVN-FWK0pVW9MscHoUiOHnjGnSo0sGhwE8hjlp1jBVtS1v-X9QaSWl5EJk6vt_qLswR59fYhFkgtIm77gm_IFlYkgpYv_km1G9ZEAfM6DvM6CXDOSmd39u_NTy-OniN80RsMY</recordid><startdate>20160801</startdate><enddate>20160801</enddate><creator>Rao, R</creator><creator>DuBois, D</creator><creator>Almon, R</creator><creator>Jusko, W J</creator><creator>Androulakis, I P</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TS</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160801</creationdate><title>Mathematical modeling of the circadian dynamics of the neuroendocrine-immune network in experimentally induced arthritis</title><author>Rao, R ; DuBois, D ; Almon, R ; Jusko, W J ; Androulakis, I P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-50d25b30690c7571de76b374533443dfaa61b837848215dba2bae0898f53af413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adrenocorticotropic Hormone - metabolism</topic><topic>Animals</topic><topic>Arthritis</topic><topic>Arthritis, Experimental - immunology</topic><topic>Arthritis, Experimental - metabolism</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - metabolism</topic><topic>Circadian rhythm</topic><topic>Circadian Rhythm - immunology</topic><topic>Corticosterone - metabolism</topic><topic>Corticotropin-Releasing Hormone - metabolism</topic><topic>Cytokines</topic><topic>Cytokines - immunology</topic><topic>Endocrine system</topic><topic>Experiments</topic><topic>Hypothalamo-Hypophyseal System - metabolism</topic><topic>Immune system</topic><topic>Mathematical models</topic><topic>Models, Theoretical</topic><topic>Pituitary-Adrenal System - metabolism</topic><topic>Receptors, Glucocorticoid - metabolism</topic><topic>Rodentia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rao, R</creatorcontrib><creatorcontrib>DuBois, D</creatorcontrib><creatorcontrib>Almon, R</creatorcontrib><creatorcontrib>Jusko, W J</creatorcontrib><creatorcontrib>Androulakis, I P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology: endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rao, R</au><au>DuBois, D</au><au>Almon, R</au><au>Jusko, W J</au><au>Androulakis, I P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mathematical modeling of the circadian dynamics of the neuroendocrine-immune network in experimentally induced arthritis</atitle><jtitle>American journal of physiology: endocrinology and metabolism</jtitle><addtitle>Am J Physiol Endocrinol Metab</addtitle><date>2016-08-01</date><risdate>2016</risdate><volume>311</volume><issue>2</issue><spage>E310</spage><epage>E324</epage><pages>E310-E324</pages><issn>0193-1849</issn><eissn>1522-1555</eissn><coden>AJPMD9</coden><abstract>The circadian dynamics of important neuroendocrine-immune mediators have been implicated in progression of rheumatoid arthritis pathophysiology, both clinically as well as in animal models. We present a mathematical model that describes the circadian interactions between mediators of the hypothalamic-pituitary-adrenal (HPA) axis and the proinflammatory cytokines. Model predictions demonstrate that chronically elevated cytokine expression results in the development of adrenal insufficiency and circadian variability in paw edema. Notably, our model also predicts that an increase in mean secretion of corticosterone (CST) after the induction of the disease is accompanied by a decrease in the amplitude of the CST oscillation. Furthermore, alterations in the phase of circadian oscillation of both cytokines and HPA axis mediators are observed. Therefore, by incorporating the circadian interactions between the neuroendocrine-immune mediators, our model is able to simulate important features of rheumatoid arthritis pathophysiology.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>27221115</pmid><doi>10.1152/ajpendo.00006.2016</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Adrenocorticotropic Hormone - metabolism Animals Arthritis Arthritis, Experimental - immunology Arthritis, Experimental - metabolism Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - metabolism Circadian rhythm Circadian Rhythm - immunology Corticosterone - metabolism Corticotropin-Releasing Hormone - metabolism Cytokines Cytokines - immunology Endocrine system Experiments Hypothalamo-Hypophyseal System - metabolism Immune system Mathematical models Models, Theoretical Pituitary-Adrenal System - metabolism Receptors, Glucocorticoid - metabolism Rodentia |
| title | Mathematical modeling of the circadian dynamics of the neuroendocrine-immune network in experimentally induced arthritis |
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