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Exogenous Tryptophan Promotes Cutaneous Wound Healing of Chronically Stressed Mice through Inhibition of TNF-α and IDO Activation
Stress prolongs the inflammatory response compromising the dermal reconstruction and wound closure. Acute stress-induced inflammation increases indoleamine 2, 3-dioxygenase-stimulated tryptophan catabolism. To investigate the role of indoleamine 2, 3-dioxygenase expression and tryptophan administrat...
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Published in: | PloS one 2015-06, Vol.10 (6), p.e0128439-e0128439 |
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description | Stress prolongs the inflammatory response compromising the dermal reconstruction and wound closure. Acute stress-induced inflammation increases indoleamine 2, 3-dioxygenase-stimulated tryptophan catabolism. To investigate the role of indoleamine 2, 3-dioxygenase expression and tryptophan administration in adverse effects of stress on cutaneous wound healing, mice were submitted to chronic restraint stress and treated with tryptophan daily until euthanasia. Excisional lesions were created on each mouse and 5 or 7 days later, the lesions were analyzed. In addition, murine skin fibroblasts were exposed to elevated epinephrine levels plus tryptophan, and fibroblast activity was evaluated. Tryptophan administration reversed the reduction of the plasma tryptophan levels and the increase in the plasma normetanephrine levels induced by stress 5 and 7 days after wounding. Five days after wounding, stress-induced increase in the protein levels of tumor necrosis factor-α and indoleamine 2, 3-dioxygenase, and this was inhibited by tryptophan. Stress-induced increase in the lipid peroxidation and the amount of the neutrophils, macrophages and T cells number was reversed by tryptophan 5 days after wounding. Tryptophan administration inhibited the reduction of myofibroblast density, collagen deposition, re-epithelialization and wound contraction induced by stress 5 days after wounding. In dermal fibroblast culture, the tryptophan administration increased the cell migration and AKT phosphorylation in cells treated with high epinephrine levels. In conclusion, tryptophan-induced reduction of inflammatory response and indoleamine 2, 3-dioxygenase expression may have accelerated cutaneous wound healing of chronically stressed mice. |
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Acute stress-induced inflammation increases indoleamine 2, 3-dioxygenase-stimulated tryptophan catabolism. To investigate the role of indoleamine 2, 3-dioxygenase expression and tryptophan administration in adverse effects of stress on cutaneous wound healing, mice were submitted to chronic restraint stress and treated with tryptophan daily until euthanasia. Excisional lesions were created on each mouse and 5 or 7 days later, the lesions were analyzed. In addition, murine skin fibroblasts were exposed to elevated epinephrine levels plus tryptophan, and fibroblast activity was evaluated. Tryptophan administration reversed the reduction of the plasma tryptophan levels and the increase in the plasma normetanephrine levels induced by stress 5 and 7 days after wounding. Five days after wounding, stress-induced increase in the protein levels of tumor necrosis factor-α and indoleamine 2, 3-dioxygenase, and this was inhibited by tryptophan. Stress-induced increase in the lipid peroxidation and the amount of the neutrophils, macrophages and T cells number was reversed by tryptophan 5 days after wounding. Tryptophan administration inhibited the reduction of myofibroblast density, collagen deposition, re-epithelialization and wound contraction induced by stress 5 days after wounding. In dermal fibroblast culture, the tryptophan administration increased the cell migration and AKT phosphorylation in cells treated with high epinephrine levels. In conclusion, tryptophan-induced reduction of inflammatory response and indoleamine 2, 3-dioxygenase expression may have accelerated cutaneous wound healing of chronically stressed mice.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0128439</identifier><identifier>PMID: 26057238</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>AKT protein ; Animals ; Catabolism ; Cell culture ; Cell migration ; Collagen ; Collagen - genetics ; Collagen - metabolism ; Contraction ; Cytokines ; Dioxygenase ; Embryology ; Epinephrine ; Euthanasia ; Fibroblasts ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Gene expression ; Histology ; Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism ; Inflammation ; Inflammatory response ; Inhibition ; Kinases ; Laboratories ; Lesions ; Leukocyte migration ; Leukocytes (neutrophilic) ; Lipid Peroxidation ; Lymphocytes ; Lymphocytes T ; Macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Metanephrine - blood ; Mice ; Neutrophils - drug effects ; Neutrophils - metabolism ; Peroxidation ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; Re-Epithelialization ; Reduction ; Rodents ; Skin ; Skin - drug effects ; Skin - injuries ; Skin - metabolism ; Stress ; Stress, Psychological - metabolism ; Stress, Psychological - pathology ; Stresses ; Studies ; Tryptophan ; Tryptophan - blood ; Tryptophan - pharmacology ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Wound healing</subject><ispartof>PloS one, 2015-06, Vol.10 (6), p.e0128439-e0128439</ispartof><rights>2015 Bandeira et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://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>2015 Bandeira et al 2015 Bandeira et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-d978b1b7a980616da1e4e16860aceb7a6b02f96a2b7e5890b03b6ee18d7ee91a3</citedby><cites>FETCH-LOGICAL-c526t-d978b1b7a980616da1e4e16860aceb7a6b02f96a2b7e5890b03b6ee18d7ee91a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1686993963/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1686993963?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26057238$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Platten, Michael</contributor><creatorcontrib>Bandeira, Luana Graziella</creatorcontrib><creatorcontrib>Bortolot, Beatriz Salari</creatorcontrib><creatorcontrib>Cecatto, Matheus Jorand</creatorcontrib><creatorcontrib>Monte-Alto-Costa, Andréa</creatorcontrib><creatorcontrib>Romana-Souza, Bruna</creatorcontrib><title>Exogenous Tryptophan Promotes Cutaneous Wound Healing of Chronically Stressed Mice through Inhibition of TNF-α and IDO Activation</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Stress prolongs the inflammatory response compromising the dermal reconstruction and wound closure. Acute stress-induced inflammation increases indoleamine 2, 3-dioxygenase-stimulated tryptophan catabolism. To investigate the role of indoleamine 2, 3-dioxygenase expression and tryptophan administration in adverse effects of stress on cutaneous wound healing, mice were submitted to chronic restraint stress and treated with tryptophan daily until euthanasia. Excisional lesions were created on each mouse and 5 or 7 days later, the lesions were analyzed. In addition, murine skin fibroblasts were exposed to elevated epinephrine levels plus tryptophan, and fibroblast activity was evaluated. Tryptophan administration reversed the reduction of the plasma tryptophan levels and the increase in the plasma normetanephrine levels induced by stress 5 and 7 days after wounding. Five days after wounding, stress-induced increase in the protein levels of tumor necrosis factor-α and indoleamine 2, 3-dioxygenase, and this was inhibited by tryptophan. Stress-induced increase in the lipid peroxidation and the amount of the neutrophils, macrophages and T cells number was reversed by tryptophan 5 days after wounding. Tryptophan administration inhibited the reduction of myofibroblast density, collagen deposition, re-epithelialization and wound contraction induced by stress 5 days after wounding. In dermal fibroblast culture, the tryptophan administration increased the cell migration and AKT phosphorylation in cells treated with high epinephrine levels. In conclusion, tryptophan-induced reduction of inflammatory response and indoleamine 2, 3-dioxygenase expression may have accelerated cutaneous wound healing of chronically stressed mice.</description><subject>AKT protein</subject><subject>Animals</subject><subject>Catabolism</subject><subject>Cell culture</subject><subject>Cell migration</subject><subject>Collagen</subject><subject>Collagen - genetics</subject><subject>Collagen - metabolism</subject><subject>Contraction</subject><subject>Cytokines</subject><subject>Dioxygenase</subject><subject>Embryology</subject><subject>Epinephrine</subject><subject>Euthanasia</subject><subject>Fibroblasts</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Gene expression</subject><subject>Histology</subject><subject>Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Inhibition</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Lesions</subject><subject>Leukocyte migration</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lipid Peroxidation</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Metanephrine - blood</subject><subject>Mice</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - metabolism</subject><subject>Peroxidation</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Re-Epithelialization</subject><subject>Reduction</subject><subject>Rodents</subject><subject>Skin</subject><subject>Skin - drug effects</subject><subject>Skin - injuries</subject><subject>Skin - metabolism</subject><subject>Stress</subject><subject>Stress, Psychological - metabolism</subject><subject>Stress, Psychological - pathology</subject><subject>Stresses</subject><subject>Studies</subject><subject>Tryptophan</subject><subject>Tryptophan - blood</subject><subject>Tryptophan - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Wound healing</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAQjRCItgv_AIElLlyy-CNx4gtStbR0pUKRWMTRmiSTXa-y9tZ2Kvbaf8Qf4TeRsNuqRcgHW_PevJnxvCR5xeiUiYK9X7veW-imW2dxShkvM6GeJMdMCZ5KTsXTB--j5CSENaW5KKV8nhxxSfOCi_I4uT376ZZoXR_Iwu-20W1XYMlX7zYuYiCzPoLFEf3hetuQC4TO2CVxLZmtvLOmhq7bkW_RYwjYkM-mRhIHpF-uyNyuTGWicXbkL76cp79_ERhU5h-vyGkdzQ2M4IvkWQtdwJeHe5J8Pz9bzC7Sy6tP89npZVrnXMa0UUVZsaoAVVLJZAMMM2SylBRqHMKyorxVEnhVYF4qWlFRSURWNgWiYiAmyZu97rZzQR--L-hRQimhpBgY8z2jcbDWW2824HfagdF_A84vNfho6g51w3IKwylaFFk2NAVlLivOay7aMoN20PpwqNZXG2xqtNFD90j0MWLNSi_djc4yyXiuBoF3BwHvrnsMUW9MqLHr9gsZ-y5kptSwx0ny9h_q_6fL9qzauxA8tvfNMKpHS91l6dFS-mCpIe31w0Huk-48JP4ADHzMrA</recordid><startdate>20150609</startdate><enddate>20150609</enddate><creator>Bandeira, Luana Graziella</creator><creator>Bortolot, Beatriz Salari</creator><creator>Cecatto, Matheus Jorand</creator><creator>Monte-Alto-Costa, Andréa</creator><creator>Romana-Souza, Bruna</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20150609</creationdate><title>Exogenous Tryptophan Promotes Cutaneous Wound Healing of Chronically Stressed Mice through Inhibition of TNF-α and IDO Activation</title><author>Bandeira, Luana Graziella ; Bortolot, Beatriz Salari ; Cecatto, Matheus Jorand ; Monte-Alto-Costa, Andréa ; Romana-Souza, Bruna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-d978b1b7a980616da1e4e16860aceb7a6b02f96a2b7e5890b03b6ee18d7ee91a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>AKT protein</topic><topic>Animals</topic><topic>Catabolism</topic><topic>Cell culture</topic><topic>Cell migration</topic><topic>Collagen</topic><topic>Collagen - genetics</topic><topic>Collagen - metabolism</topic><topic>Contraction</topic><topic>Cytokines</topic><topic>Dioxygenase</topic><topic>Embryology</topic><topic>Epinephrine</topic><topic>Euthanasia</topic><topic>Fibroblasts</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Gene expression</topic><topic>Histology</topic><topic>Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Inhibition</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Lesions</topic><topic>Leukocyte migration</topic><topic>Leukocytes (neutrophilic)</topic><topic>Lipid Peroxidation</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Metanephrine - blood</topic><topic>Mice</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - metabolism</topic><topic>Peroxidation</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - 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Acute stress-induced inflammation increases indoleamine 2, 3-dioxygenase-stimulated tryptophan catabolism. To investigate the role of indoleamine 2, 3-dioxygenase expression and tryptophan administration in adverse effects of stress on cutaneous wound healing, mice were submitted to chronic restraint stress and treated with tryptophan daily until euthanasia. Excisional lesions were created on each mouse and 5 or 7 days later, the lesions were analyzed. In addition, murine skin fibroblasts were exposed to elevated epinephrine levels plus tryptophan, and fibroblast activity was evaluated. Tryptophan administration reversed the reduction of the plasma tryptophan levels and the increase in the plasma normetanephrine levels induced by stress 5 and 7 days after wounding. Five days after wounding, stress-induced increase in the protein levels of tumor necrosis factor-α and indoleamine 2, 3-dioxygenase, and this was inhibited by tryptophan. Stress-induced increase in the lipid peroxidation and the amount of the neutrophils, macrophages and T cells number was reversed by tryptophan 5 days after wounding. Tryptophan administration inhibited the reduction of myofibroblast density, collagen deposition, re-epithelialization and wound contraction induced by stress 5 days after wounding. In dermal fibroblast culture, the tryptophan administration increased the cell migration and AKT phosphorylation in cells treated with high epinephrine levels. In conclusion, tryptophan-induced reduction of inflammatory response and indoleamine 2, 3-dioxygenase expression may have accelerated cutaneous wound healing of chronically stressed mice.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26057238</pmid><doi>10.1371/journal.pone.0128439</doi><oa>free_for_read</oa></addata></record> |
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subjects | AKT protein Animals Catabolism Cell culture Cell migration Collagen Collagen - genetics Collagen - metabolism Contraction Cytokines Dioxygenase Embryology Epinephrine Euthanasia Fibroblasts Fibroblasts - drug effects Fibroblasts - metabolism Gene expression Histology Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism Inflammation Inflammatory response Inhibition Kinases Laboratories Lesions Leukocyte migration Leukocytes (neutrophilic) Lipid Peroxidation Lymphocytes Lymphocytes T Macrophages Macrophages - drug effects Macrophages - metabolism Male Metanephrine - blood Mice Neutrophils - drug effects Neutrophils - metabolism Peroxidation Phosphorylation Proto-Oncogene Proteins c-akt - metabolism Re-Epithelialization Reduction Rodents Skin Skin - drug effects Skin - injuries Skin - metabolism Stress Stress, Psychological - metabolism Stress, Psychological - pathology Stresses Studies Tryptophan Tryptophan - blood Tryptophan - pharmacology Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α Wound healing |
title | Exogenous Tryptophan Promotes Cutaneous Wound Healing of Chronically Stressed Mice through Inhibition of TNF-α and IDO Activation |
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