Sex Steroid Regulation of Macrophage Migration Inhibitory Factor in Normal and Inflamed Colon in the Female Rat
Background & Aims: Sex steroids influence IBD symptoms. Macrophage migration inhibitory factor (MIF), a target of sex steroids in other inflammatory models, promotes interleukin (IL)-1β and tumor necrosis factor (TNF)-α release in colitis. We investigated whether estradiol and progesterone influ...
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| Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2007-03, Vol.132 (3), p.982-993 |
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| creator | Houdeau, Eric Moriez, Raphael Leveque, Mathilde Salvador–Cartier, Christel Waget, Aurelie Leng, Lin Bueno, Lionel Bucala, Richard Fioramonti, Jean |
| description | Background & Aims: Sex steroids influence IBD symptoms. Macrophage migration inhibitory factor (MIF), a target of sex steroids in other inflammatory models, promotes interleukin (IL)-1β and tumor necrosis factor (TNF)-α release in colitis. We investigated whether estradiol and progesterone influence MIF, IL-1β, and TNF-α production in experimental colitis. Methods: Colonic MIF, IL-1β, and TNF-α levels were measured in cyclic and ovariectomized rats, with or without estradiol benzoate (EB) or progesterone (P) replacement. MIF distribution was assessed by immunohistochemistry. Cytokines, myeloperoxidase activity, macroscopic damage, and plasma corticosterone were assessed 24 hours after intrarectal trinitrobenzene sulfonic acid (TNBS), with and without neutralizing anti-MIF antibody. Effects of EB and P on myeloperoxidase activity and MIF concentration were also assessed at 7 days in dextran sulfate sodium-induced colitis. Results: Basal IL-1β and TNF-α contents did not fluctuate during the estrous cycle, while MIF concentrations increased from estrus (estrogen dominance) to metestrus (P dominance; P < .05). EB and P treatment mimicked these effects in ovariectomized rats, and similarly altered MIF immunostaining. Progesterone dominance aggravated TNBS colitis in comparison with estrogen. Progesterone enhanced TNBS-induced MIF ( P < .001) and TNF-α ( P < .01) production, while EB decreased MIF ( P < .01) and IL-β levels ( P < .01). Anti-MIF antibody prevented P-mediated up-regulation of TNF-α, improved TNBS colitis, and enhanced plasma corticosterone. At 7 days after dextran sulfate sodium, EB decreased myeloperoxidase activity and MIF concentration, while P had no effect. Conclusions: Estrogen decreases while progesterone increases MIF production in the female rat colon. Changes in basal MIF contents may affect colon susceptibility to inflammation, by modulating TNF-α and IL-1β production during early stages of colitis. |
| doi_str_mv | 10.1053/j.gastro.2006.12.028 |
| format | Article |
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Macrophage migration inhibitory factor (MIF), a target of sex steroids in other inflammatory models, promotes interleukin (IL)-1β and tumor necrosis factor (TNF)-α release in colitis. We investigated whether estradiol and progesterone influence MIF, IL-1β, and TNF-α production in experimental colitis. Methods: Colonic MIF, IL-1β, and TNF-α levels were measured in cyclic and ovariectomized rats, with or without estradiol benzoate (EB) or progesterone (P) replacement. MIF distribution was assessed by immunohistochemistry. Cytokines, myeloperoxidase activity, macroscopic damage, and plasma corticosterone were assessed 24 hours after intrarectal trinitrobenzene sulfonic acid (TNBS), with and without neutralizing anti-MIF antibody. Effects of EB and P on myeloperoxidase activity and MIF concentration were also assessed at 7 days in dextran sulfate sodium-induced colitis. Results: Basal IL-1β and TNF-α contents did not fluctuate during the estrous cycle, while MIF concentrations increased from estrus (estrogen dominance) to metestrus (P dominance; P < .05). EB and P treatment mimicked these effects in ovariectomized rats, and similarly altered MIF immunostaining. Progesterone dominance aggravated TNBS colitis in comparison with estrogen. Progesterone enhanced TNBS-induced MIF ( P < .001) and TNF-α ( P < .01) production, while EB decreased MIF ( P < .01) and IL-β levels ( P < .01). Anti-MIF antibody prevented P-mediated up-regulation of TNF-α, improved TNBS colitis, and enhanced plasma corticosterone. At 7 days after dextran sulfate sodium, EB decreased myeloperoxidase activity and MIF concentration, while P had no effect. Conclusions: Estrogen decreases while progesterone increases MIF production in the female rat colon. Changes in basal MIF contents may affect colon susceptibility to inflammation, by modulating TNF-α and IL-1β production during early stages of colitis.]]></description><identifier>ISSN: 0016-5085</identifier><identifier>EISSN: 1528-0012</identifier><identifier>DOI: 10.1053/j.gastro.2006.12.028</identifier><identifier>PMID: 17324399</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Antibodies, Monoclonal - pharmacology ; Colitis - chemically induced ; Colitis - metabolism ; Colitis - pathology ; Colon - drug effects ; Colon - metabolism ; Colon - pathology ; Corticosterone - blood ; Dextran Sulfate ; Disease Models, Animal ; Estradiol - analogs & derivatives ; Estradiol - metabolism ; Estrous Cycle - metabolism ; Female ; Gastroenterology and Hepatology ; Gonadal Steroid Hormones - metabolism ; Gonadal Steroid Hormones - pharmacology ; Immunohistochemistry ; Interleukin-1beta - metabolism ; Intramolecular Oxidoreductases - antagonists & inhibitors ; Intramolecular Oxidoreductases - immunology ; Intramolecular Oxidoreductases - metabolism ; Life Sciences ; Macrophage Migration-Inhibitory Factors - antagonists & inhibitors ; Macrophage Migration-Inhibitory Factors - immunology ; Macrophage Migration-Inhibitory Factors - metabolism ; Ovariectomy ; Peroxidase - metabolism ; Progesterone - metabolism ; Rats ; Rats, Wistar ; Severity of Illness Index ; Sex Factors ; Time Factors ; Trinitrobenzenesulfonic Acid ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 2007-03, Vol.132 (3), p.982-993</ispartof><rights>AGA Institute</rights><rights>2007 AGA Institute</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c495t-4ca3d494f44257133aa5f0438bf42bd4f5254a3ae9cd1ce5fbc4efe1c9d121f83</citedby><cites>FETCH-LOGICAL-c495t-4ca3d494f44257133aa5f0438bf42bd4f5254a3ae9cd1ce5fbc4efe1c9d121f83</cites><orcidid>0009-0005-4813-8396 ; 0000-0003-1971-9827 ; 0000-0001-5783-5736</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0016508506026783$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17324399$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-01608727$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Houdeau, Eric</creatorcontrib><creatorcontrib>Moriez, Raphael</creatorcontrib><creatorcontrib>Leveque, Mathilde</creatorcontrib><creatorcontrib>Salvador–Cartier, Christel</creatorcontrib><creatorcontrib>Waget, Aurelie</creatorcontrib><creatorcontrib>Leng, Lin</creatorcontrib><creatorcontrib>Bueno, Lionel</creatorcontrib><creatorcontrib>Bucala, Richard</creatorcontrib><creatorcontrib>Fioramonti, Jean</creatorcontrib><title>Sex Steroid Regulation of Macrophage Migration Inhibitory Factor in Normal and Inflamed Colon in the Female Rat</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description><![CDATA[Background & Aims: Sex steroids influence IBD symptoms. Macrophage migration inhibitory factor (MIF), a target of sex steroids in other inflammatory models, promotes interleukin (IL)-1β and tumor necrosis factor (TNF)-α release in colitis. We investigated whether estradiol and progesterone influence MIF, IL-1β, and TNF-α production in experimental colitis. Methods: Colonic MIF, IL-1β, and TNF-α levels were measured in cyclic and ovariectomized rats, with or without estradiol benzoate (EB) or progesterone (P) replacement. MIF distribution was assessed by immunohistochemistry. Cytokines, myeloperoxidase activity, macroscopic damage, and plasma corticosterone were assessed 24 hours after intrarectal trinitrobenzene sulfonic acid (TNBS), with and without neutralizing anti-MIF antibody. Effects of EB and P on myeloperoxidase activity and MIF concentration were also assessed at 7 days in dextran sulfate sodium-induced colitis. Results: Basal IL-1β and TNF-α contents did not fluctuate during the estrous cycle, while MIF concentrations increased from estrus (estrogen dominance) to metestrus (P dominance; P < .05). EB and P treatment mimicked these effects in ovariectomized rats, and similarly altered MIF immunostaining. Progesterone dominance aggravated TNBS colitis in comparison with estrogen. Progesterone enhanced TNBS-induced MIF ( P < .001) and TNF-α ( P < .01) production, while EB decreased MIF ( P < .01) and IL-β levels ( P < .01). Anti-MIF antibody prevented P-mediated up-regulation of TNF-α, improved TNBS colitis, and enhanced plasma corticosterone. At 7 days after dextran sulfate sodium, EB decreased myeloperoxidase activity and MIF concentration, while P had no effect. Conclusions: Estrogen decreases while progesterone increases MIF production in the female rat colon. Changes in basal MIF contents may affect colon susceptibility to inflammation, by modulating TNF-α and IL-1β production during early stages of colitis.]]></description><subject>Animals</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Colitis - chemically induced</subject><subject>Colitis - metabolism</subject><subject>Colitis - pathology</subject><subject>Colon - drug effects</subject><subject>Colon - metabolism</subject><subject>Colon - pathology</subject><subject>Corticosterone - blood</subject><subject>Dextran Sulfate</subject><subject>Disease Models, Animal</subject><subject>Estradiol - analogs & derivatives</subject><subject>Estradiol - metabolism</subject><subject>Estrous Cycle - metabolism</subject><subject>Female</subject><subject>Gastroenterology and Hepatology</subject><subject>Gonadal Steroid Hormones - metabolism</subject><subject>Gonadal Steroid Hormones - pharmacology</subject><subject>Immunohistochemistry</subject><subject>Interleukin-1beta - metabolism</subject><subject>Intramolecular Oxidoreductases - antagonists & inhibitors</subject><subject>Intramolecular Oxidoreductases - immunology</subject><subject>Intramolecular Oxidoreductases - metabolism</subject><subject>Life Sciences</subject><subject>Macrophage Migration-Inhibitory Factors - antagonists & inhibitors</subject><subject>Macrophage Migration-Inhibitory Factors - immunology</subject><subject>Macrophage Migration-Inhibitory Factors - metabolism</subject><subject>Ovariectomy</subject><subject>Peroxidase - metabolism</subject><subject>Progesterone - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Severity of Illness Index</subject><subject>Sex Factors</subject><subject>Time Factors</subject><subject>Trinitrobenzenesulfonic Acid</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0016-5085</issn><issn>1528-0012</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU-P0zAQxS0EYsvCN0DIVw4J_tskF6RVtWVX6oK0hbM1ccatSxpXdrqi3x5HWYHEhdNIM-_N6P2GkPeclZxp-elQ7iCNMZSCsWXJRclE_YIsuBZ1wRgXL8kil2WhWa2vyJuUDoyxRtb8NbnilRRKNs2ChC3-otsRY_AdfcTduYfRh4EGRx_AxnDaww7pg9_FuX8_7H3rxxAvdA02V-oH-jXEI_QUhi7PXQ9H7Ogq9Fmeh-Me6RrzHOkjjG_JKwd9wnfP9Zr8WN9-X90Vm29f7lc3m8KqRo-FsiA71SinlNAVlxJAO6Zk3Tol2k45LbQCCdjYjlvUrrUKHXLbdFxwV8tr8nHeu4fenKI_QryYAN7c3WzM1MtoWF2J6olnrZq1OW9KEd0fA2dmYm0OZmZtJtaGC5NZZ9uH2XY6tznxX9Mz3Cz4PAswB33yGE2yHgeLnY9oR9MF_78L_y6wvR-8hf4nXjAdwjkOGaLhJmWD2U7_nt7Nlkwsq1rK310jpv4</recordid><startdate>20070301</startdate><enddate>20070301</enddate><creator>Houdeau, Eric</creator><creator>Moriez, Raphael</creator><creator>Leveque, Mathilde</creator><creator>Salvador–Cartier, Christel</creator><creator>Waget, Aurelie</creator><creator>Leng, Lin</creator><creator>Bueno, Lionel</creator><creator>Bucala, Richard</creator><creator>Fioramonti, Jean</creator><general>Elsevier Inc</general><general>Elsevier</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>1XC</scope><orcidid>https://orcid.org/0009-0005-4813-8396</orcidid><orcidid>https://orcid.org/0000-0003-1971-9827</orcidid><orcidid>https://orcid.org/0000-0001-5783-5736</orcidid></search><sort><creationdate>20070301</creationdate><title>Sex Steroid Regulation of Macrophage Migration Inhibitory Factor in Normal and Inflamed Colon in the Female Rat</title><author>Houdeau, Eric ; Moriez, Raphael ; Leveque, Mathilde ; Salvador–Cartier, Christel ; Waget, Aurelie ; Leng, Lin ; Bueno, Lionel ; Bucala, Richard ; Fioramonti, Jean</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c495t-4ca3d494f44257133aa5f0438bf42bd4f5254a3ae9cd1ce5fbc4efe1c9d121f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Colitis - chemically induced</topic><topic>Colitis - metabolism</topic><topic>Colitis - pathology</topic><topic>Colon - drug effects</topic><topic>Colon - metabolism</topic><topic>Colon - pathology</topic><topic>Corticosterone - blood</topic><topic>Dextran Sulfate</topic><topic>Disease Models, Animal</topic><topic>Estradiol - analogs & derivatives</topic><topic>Estradiol - metabolism</topic><topic>Estrous Cycle - metabolism</topic><topic>Female</topic><topic>Gastroenterology and Hepatology</topic><topic>Gonadal Steroid Hormones - metabolism</topic><topic>Gonadal Steroid Hormones - pharmacology</topic><topic>Immunohistochemistry</topic><topic>Interleukin-1beta - metabolism</topic><topic>Intramolecular Oxidoreductases - antagonists & inhibitors</topic><topic>Intramolecular Oxidoreductases - immunology</topic><topic>Intramolecular Oxidoreductases - metabolism</topic><topic>Life Sciences</topic><topic>Macrophage Migration-Inhibitory Factors - antagonists & inhibitors</topic><topic>Macrophage Migration-Inhibitory Factors - immunology</topic><topic>Macrophage Migration-Inhibitory Factors - metabolism</topic><topic>Ovariectomy</topic><topic>Peroxidase - metabolism</topic><topic>Progesterone - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Severity of Illness Index</topic><topic>Sex Factors</topic><topic>Time Factors</topic><topic>Trinitrobenzenesulfonic Acid</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Houdeau, Eric</creatorcontrib><creatorcontrib>Moriez, Raphael</creatorcontrib><creatorcontrib>Leveque, Mathilde</creatorcontrib><creatorcontrib>Salvador–Cartier, Christel</creatorcontrib><creatorcontrib>Waget, Aurelie</creatorcontrib><creatorcontrib>Leng, Lin</creatorcontrib><creatorcontrib>Bueno, Lionel</creatorcontrib><creatorcontrib>Bucala, Richard</creatorcontrib><creatorcontrib>Fioramonti, Jean</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Houdeau, Eric</au><au>Moriez, Raphael</au><au>Leveque, Mathilde</au><au>Salvador–Cartier, Christel</au><au>Waget, Aurelie</au><au>Leng, Lin</au><au>Bueno, Lionel</au><au>Bucala, Richard</au><au>Fioramonti, Jean</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sex Steroid Regulation of Macrophage Migration Inhibitory Factor in Normal and Inflamed Colon in the Female Rat</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>2007-03-01</date><risdate>2007</risdate><volume>132</volume><issue>3</issue><spage>982</spage><epage>993</epage><pages>982-993</pages><issn>0016-5085</issn><eissn>1528-0012</eissn><abstract><![CDATA[Background & Aims: Sex steroids influence IBD symptoms. Macrophage migration inhibitory factor (MIF), a target of sex steroids in other inflammatory models, promotes interleukin (IL)-1β and tumor necrosis factor (TNF)-α release in colitis. We investigated whether estradiol and progesterone influence MIF, IL-1β, and TNF-α production in experimental colitis. Methods: Colonic MIF, IL-1β, and TNF-α levels were measured in cyclic and ovariectomized rats, with or without estradiol benzoate (EB) or progesterone (P) replacement. MIF distribution was assessed by immunohistochemistry. Cytokines, myeloperoxidase activity, macroscopic damage, and plasma corticosterone were assessed 24 hours after intrarectal trinitrobenzene sulfonic acid (TNBS), with and without neutralizing anti-MIF antibody. Effects of EB and P on myeloperoxidase activity and MIF concentration were also assessed at 7 days in dextran sulfate sodium-induced colitis. Results: Basal IL-1β and TNF-α contents did not fluctuate during the estrous cycle, while MIF concentrations increased from estrus (estrogen dominance) to metestrus (P dominance; P < .05). EB and P treatment mimicked these effects in ovariectomized rats, and similarly altered MIF immunostaining. Progesterone dominance aggravated TNBS colitis in comparison with estrogen. Progesterone enhanced TNBS-induced MIF ( P < .001) and TNF-α ( P < .01) production, while EB decreased MIF ( P < .01) and IL-β levels ( P < .01). Anti-MIF antibody prevented P-mediated up-regulation of TNF-α, improved TNBS colitis, and enhanced plasma corticosterone. At 7 days after dextran sulfate sodium, EB decreased myeloperoxidase activity and MIF concentration, while P had no effect. Conclusions: Estrogen decreases while progesterone increases MIF production in the female rat colon. Changes in basal MIF contents may affect colon susceptibility to inflammation, by modulating TNF-α and IL-1β production during early stages of colitis.]]></abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17324399</pmid><doi>10.1053/j.gastro.2006.12.028</doi><tpages>12</tpages><orcidid>https://orcid.org/0009-0005-4813-8396</orcidid><orcidid>https://orcid.org/0000-0003-1971-9827</orcidid><orcidid>https://orcid.org/0000-0001-5783-5736</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Gastroenterology (New York, N.Y. 1943), 2007-03, Vol.132 (3), p.982-993 |
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| subjects | Animals Antibodies, Monoclonal - pharmacology Colitis - chemically induced Colitis - metabolism Colitis - pathology Colon - drug effects Colon - metabolism Colon - pathology Corticosterone - blood Dextran Sulfate Disease Models, Animal Estradiol - analogs & derivatives Estradiol - metabolism Estrous Cycle - metabolism Female Gastroenterology and Hepatology Gonadal Steroid Hormones - metabolism Gonadal Steroid Hormones - pharmacology Immunohistochemistry Interleukin-1beta - metabolism Intramolecular Oxidoreductases - antagonists & inhibitors Intramolecular Oxidoreductases - immunology Intramolecular Oxidoreductases - metabolism Life Sciences Macrophage Migration-Inhibitory Factors - antagonists & inhibitors Macrophage Migration-Inhibitory Factors - immunology Macrophage Migration-Inhibitory Factors - metabolism Ovariectomy Peroxidase - metabolism Progesterone - metabolism Rats Rats, Wistar Severity of Illness Index Sex Factors Time Factors Trinitrobenzenesulfonic Acid Tumor Necrosis Factor-alpha - metabolism |
| title | Sex Steroid Regulation of Macrophage Migration Inhibitory Factor in Normal and Inflamed Colon in the Female Rat |
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