Antiinflammatory effect of androgen receptor activation in human benign prostatic hyperplasia cells
Progression of benign prostatic hyperplasia (BPH) involves chronic inflammation and immune dysregulation. Preclinical studies have demonstrated that prostate inflammation and tissue remodeling are exacerbated by hypogonadism and prevented by testosterone supplementation. We now investigated whether,...
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| Veröffentlicht in: | Journal of endocrinology 2012-07, Vol.214 (1), p.31-43 |
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| creator | Vignozzi, Linda Cellai, Ilaria Santi, Raffaella Lombardelli, Letizia Morelli, Annamaria Comeglio, Paolo Filippi, Sandra Logiodice, Federica Carini, Marco Nesi, Gabriella Gacci, Mauro Piccinni, Marie-Pierre Adorini, Luciano Maggi, Mario |
| description | Progression of benign prostatic hyperplasia (BPH) involves chronic inflammation and immune dysregulation. Preclinical studies have demonstrated that prostate inflammation and tissue remodeling are exacerbated by hypogonadism and prevented by testosterone supplementation. We now investigated whether, in humans, hypogonadism was associated with more severe BPH inflammation and the in vitro effect of the selective androgen receptor agonist dihydrotestosterone (DHT) on cultures of stromal cells derived from BPH patients (hBPH). Histological analysis of inflammatory infiltrates in prostatectomy specimens from a cohort of BPH patients and correlation with serum testosterone level was performed. Even after adjusting for confounding factors, hypogonadism was associated with a fivefold increased risk of intraprostatic inflammation, which was also more severe than that observed in eugonadal BPH patients. Triggering hBPH cells by inflammatory stimuli (tumor necrosis factor α, lipopolysaccharide, or CD4+T cells) induced abundant secretion of inflammatory/growth factors (interleukin 6 (IL6), IL8, and basic fibroblast growth factor (bFGF)). Co-culture of CD4+T cells with hBPH cells induced secretion of Th1 inducer (IL12), Th1-recruiting chemokine (interferon γ inducible protein 10, IP10), and Th2 (IL9)- and Th17 (IL17)-specific cytokines. Pretreatment with DHT inhibited NF-κB activation and suppressed secretion of several inflammatory/growth factors, with the most pronounced effects on IL8, IL6, and bFGF. Reduced inflammatory cytokine production by testosterone cells, an increase in IL10, and a significant reduction of testosterone cells proliferation suggested that DHT exerted a broad antiinflammatory effect on testosterone cells. In conclusion, our data demonstrate that DHT exerts an immune regulatory role on human prostatic stromal cells, inhibiting their potential to actively induce and/or sustain autoimmune and inflammatory responses. |
| doi_str_mv | 10.1530/JOE-12-0142 |
| format | Article |
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Preclinical studies have demonstrated that prostate inflammation and tissue remodeling are exacerbated by hypogonadism and prevented by testosterone supplementation. We now investigated whether, in humans, hypogonadism was associated with more severe BPH inflammation and the in vitro effect of the selective androgen receptor agonist dihydrotestosterone (DHT) on cultures of stromal cells derived from BPH patients (hBPH). Histological analysis of inflammatory infiltrates in prostatectomy specimens from a cohort of BPH patients and correlation with serum testosterone level was performed. Even after adjusting for confounding factors, hypogonadism was associated with a fivefold increased risk of intraprostatic inflammation, which was also more severe than that observed in eugonadal BPH patients. Triggering hBPH cells by inflammatory stimuli (tumor necrosis factor α, lipopolysaccharide, or CD4+T cells) induced abundant secretion of inflammatory/growth factors (interleukin 6 (IL6), IL8, and basic fibroblast growth factor (bFGF)). Co-culture of CD4+T cells with hBPH cells induced secretion of Th1 inducer (IL12), Th1-recruiting chemokine (interferon γ inducible protein 10, IP10), and Th2 (IL9)- and Th17 (IL17)-specific cytokines. Pretreatment with DHT inhibited NF-κB activation and suppressed secretion of several inflammatory/growth factors, with the most pronounced effects on IL8, IL6, and bFGF. Reduced inflammatory cytokine production by testosterone cells, an increase in IL10, and a significant reduction of testosterone cells proliferation suggested that DHT exerted a broad antiinflammatory effect on testosterone cells. In conclusion, our data demonstrate that DHT exerts an immune regulatory role on human prostatic stromal cells, inhibiting their potential to actively induce and/or sustain autoimmune and inflammatory responses.</description><identifier>ISSN: 0022-0795</identifier><identifier>EISSN: 1479-6805</identifier><identifier>DOI: 10.1530/JOE-12-0142</identifier><identifier>PMID: 22562653</identifier><identifier>CODEN: JOENAK</identifier><language>eng</language><publisher>Bristol: BioScientifica</publisher><subject>Aged ; Aged, 80 and over ; Androgens - pharmacology ; Biological and medical sciences ; CD4-Positive T-Lymphocytes - drug effects ; CD4-Positive T-Lymphocytes - metabolism ; Cell Proliferation - drug effects ; Cells, Cultured ; Coculture Techniques ; Cohort Studies ; Cyclooxygenase 2 - genetics ; Cytokines - metabolism ; Dihydrotestosterone - pharmacology ; Fundamental and applied biological sciences. Psychology ; Gene Expression - drug effects ; Gynecology. Andrology. Obstetrics ; Humans ; Inflammation Mediators - metabolism ; Intercellular Signaling Peptides and Proteins - metabolism ; Lymphocyte Activation - drug effects ; Male ; Male genital diseases ; Medical sciences ; Microscopy, Fluorescence ; Middle Aged ; Nephrology. Urinary tract diseases ; Prostatic Hyperplasia - blood ; Prostatic Hyperplasia - metabolism ; Prostatic Hyperplasia - pathology ; Receptors, Androgen - metabolism ; Regular papers ; Testosterone - blood ; Testosterone - metabolism ; Transcription Factor RelA - metabolism ; Tumor Necrosis Factor-alpha - pharmacology ; Tumors ; Tumors of the urinary system ; Urinary tract. Prostate gland ; Vertebrates: endocrinology</subject><ispartof>Journal of endocrinology, 2012-07, Vol.214 (1), p.31-43</ispartof><rights>2012 Society for Endocrinology</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b464t-49d347a6761d9976a3cd5a097dbf2fff061fdaf4519efc72f0b77f1b3243bbbe3</citedby><cites>FETCH-LOGICAL-b464t-49d347a6761d9976a3cd5a097dbf2fff061fdaf4519efc72f0b77f1b3243bbbe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26137154$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22562653$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vignozzi, Linda</creatorcontrib><creatorcontrib>Cellai, Ilaria</creatorcontrib><creatorcontrib>Santi, Raffaella</creatorcontrib><creatorcontrib>Lombardelli, Letizia</creatorcontrib><creatorcontrib>Morelli, Annamaria</creatorcontrib><creatorcontrib>Comeglio, Paolo</creatorcontrib><creatorcontrib>Filippi, Sandra</creatorcontrib><creatorcontrib>Logiodice, Federica</creatorcontrib><creatorcontrib>Carini, Marco</creatorcontrib><creatorcontrib>Nesi, Gabriella</creatorcontrib><creatorcontrib>Gacci, Mauro</creatorcontrib><creatorcontrib>Piccinni, Marie-Pierre</creatorcontrib><creatorcontrib>Adorini, Luciano</creatorcontrib><creatorcontrib>Maggi, Mario</creatorcontrib><title>Antiinflammatory effect of androgen receptor activation in human benign prostatic hyperplasia cells</title><title>Journal of endocrinology</title><addtitle>J Endocrinol</addtitle><description>Progression of benign prostatic hyperplasia (BPH) involves chronic inflammation and immune dysregulation. Preclinical studies have demonstrated that prostate inflammation and tissue remodeling are exacerbated by hypogonadism and prevented by testosterone supplementation. We now investigated whether, in humans, hypogonadism was associated with more severe BPH inflammation and the in vitro effect of the selective androgen receptor agonist dihydrotestosterone (DHT) on cultures of stromal cells derived from BPH patients (hBPH). Histological analysis of inflammatory infiltrates in prostatectomy specimens from a cohort of BPH patients and correlation with serum testosterone level was performed. Even after adjusting for confounding factors, hypogonadism was associated with a fivefold increased risk of intraprostatic inflammation, which was also more severe than that observed in eugonadal BPH patients. Triggering hBPH cells by inflammatory stimuli (tumor necrosis factor α, lipopolysaccharide, or CD4+T cells) induced abundant secretion of inflammatory/growth factors (interleukin 6 (IL6), IL8, and basic fibroblast growth factor (bFGF)). Co-culture of CD4+T cells with hBPH cells induced secretion of Th1 inducer (IL12), Th1-recruiting chemokine (interferon γ inducible protein 10, IP10), and Th2 (IL9)- and Th17 (IL17)-specific cytokines. Pretreatment with DHT inhibited NF-κB activation and suppressed secretion of several inflammatory/growth factors, with the most pronounced effects on IL8, IL6, and bFGF. Reduced inflammatory cytokine production by testosterone cells, an increase in IL10, and a significant reduction of testosterone cells proliferation suggested that DHT exerted a broad antiinflammatory effect on testosterone cells. In conclusion, our data demonstrate that DHT exerts an immune regulatory role on human prostatic stromal cells, inhibiting their potential to actively induce and/or sustain autoimmune and inflammatory responses.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Androgens - pharmacology</subject><subject>Biological and medical sciences</subject><subject>CD4-Positive T-Lymphocytes - drug effects</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Coculture Techniques</subject><subject>Cohort Studies</subject><subject>Cyclooxygenase 2 - genetics</subject><subject>Cytokines - metabolism</subject><subject>Dihydrotestosterone - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression - drug effects</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Inflammation Mediators - metabolism</subject><subject>Intercellular Signaling Peptides and Proteins - metabolism</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Male</subject><subject>Male genital diseases</subject><subject>Medical sciences</subject><subject>Microscopy, Fluorescence</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Prostatic Hyperplasia - blood</subject><subject>Prostatic Hyperplasia - metabolism</subject><subject>Prostatic Hyperplasia - pathology</subject><subject>Receptors, Androgen - metabolism</subject><subject>Regular papers</subject><subject>Testosterone - blood</subject><subject>Testosterone - metabolism</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><subject>Vertebrates: endocrinology</subject><issn>0022-0795</issn><issn>1479-6805</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90E2LFDEQBuAgijuunrxLLoIgral82sdlWb9Y2Iuem0o6tRvpTrdJjzD_3gwz6s1ToOqh8vIy9hLEOzBKvP96d9OB7ARo-YjtQLu-sx-Eecx2Qsg2d725YM9q_SEEGHDqKbuQ0lhpjdqxcJW3lDJNOM-4LeXAI1EMG1-IYx7Lch8zLzHEtS05hi39wi0tmafMH_YzZu5jTveZr2WpW1sF_nBYY1knrAl5iNNUn7MnhFONL87vJfv-8ebb9efu9u7Tl-ur285rq7dO96PSDq2zMPa9s6jCaFD0bvQkiUhYoBFJG-gjBSdJeOcIvJJaee-jumRvTndblp_7WLdhTvWYAHNc9nUAoQwI20vT6NsTDS12LZGGtaQZy6Gh4djq0FodQA7HVpt-dT6893Mc_9o_NTbw-gywBpyoYA6p_nMWlAOjm4OT82mpIcXWPaWA__38N0z7kV4</recordid><startdate>20120701</startdate><enddate>20120701</enddate><creator>Vignozzi, Linda</creator><creator>Cellai, Ilaria</creator><creator>Santi, Raffaella</creator><creator>Lombardelli, Letizia</creator><creator>Morelli, Annamaria</creator><creator>Comeglio, Paolo</creator><creator>Filippi, Sandra</creator><creator>Logiodice, Federica</creator><creator>Carini, Marco</creator><creator>Nesi, Gabriella</creator><creator>Gacci, Mauro</creator><creator>Piccinni, Marie-Pierre</creator><creator>Adorini, Luciano</creator><creator>Maggi, Mario</creator><general>BioScientifica</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20120701</creationdate><title>Antiinflammatory effect of androgen receptor activation in human benign prostatic hyperplasia cells</title><author>Vignozzi, Linda ; Cellai, Ilaria ; Santi, Raffaella ; Lombardelli, Letizia ; Morelli, Annamaria ; Comeglio, Paolo ; Filippi, Sandra ; Logiodice, Federica ; Carini, Marco ; Nesi, Gabriella ; Gacci, Mauro ; Piccinni, Marie-Pierre ; Adorini, Luciano ; Maggi, Mario</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b464t-49d347a6761d9976a3cd5a097dbf2fff061fdaf4519efc72f0b77f1b3243bbbe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Androgens - pharmacology</topic><topic>Biological and medical sciences</topic><topic>CD4-Positive T-Lymphocytes - drug effects</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Coculture Techniques</topic><topic>Cohort Studies</topic><topic>Cyclooxygenase 2 - genetics</topic><topic>Cytokines - metabolism</topic><topic>Dihydrotestosterone - pharmacology</topic><topic>Fundamental and applied biological sciences. 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Preclinical studies have demonstrated that prostate inflammation and tissue remodeling are exacerbated by hypogonadism and prevented by testosterone supplementation. We now investigated whether, in humans, hypogonadism was associated with more severe BPH inflammation and the in vitro effect of the selective androgen receptor agonist dihydrotestosterone (DHT) on cultures of stromal cells derived from BPH patients (hBPH). Histological analysis of inflammatory infiltrates in prostatectomy specimens from a cohort of BPH patients and correlation with serum testosterone level was performed. Even after adjusting for confounding factors, hypogonadism was associated with a fivefold increased risk of intraprostatic inflammation, which was also more severe than that observed in eugonadal BPH patients. Triggering hBPH cells by inflammatory stimuli (tumor necrosis factor α, lipopolysaccharide, or CD4+T cells) induced abundant secretion of inflammatory/growth factors (interleukin 6 (IL6), IL8, and basic fibroblast growth factor (bFGF)). Co-culture of CD4+T cells with hBPH cells induced secretion of Th1 inducer (IL12), Th1-recruiting chemokine (interferon γ inducible protein 10, IP10), and Th2 (IL9)- and Th17 (IL17)-specific cytokines. Pretreatment with DHT inhibited NF-κB activation and suppressed secretion of several inflammatory/growth factors, with the most pronounced effects on IL8, IL6, and bFGF. Reduced inflammatory cytokine production by testosterone cells, an increase in IL10, and a significant reduction of testosterone cells proliferation suggested that DHT exerted a broad antiinflammatory effect on testosterone cells. In conclusion, our data demonstrate that DHT exerts an immune regulatory role on human prostatic stromal cells, inhibiting their potential to actively induce and/or sustain autoimmune and inflammatory responses.</abstract><cop>Bristol</cop><pub>BioScientifica</pub><pmid>22562653</pmid><doi>10.1530/JOE-12-0142</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aged, 80 and over Androgens - pharmacology Biological and medical sciences CD4-Positive T-Lymphocytes - drug effects CD4-Positive T-Lymphocytes - metabolism Cell Proliferation - drug effects Cells, Cultured Coculture Techniques Cohort Studies Cyclooxygenase 2 - genetics Cytokines - metabolism Dihydrotestosterone - pharmacology Fundamental and applied biological sciences. Psychology Gene Expression - drug effects Gynecology. Andrology. Obstetrics Humans Inflammation Mediators - metabolism Intercellular Signaling Peptides and Proteins - metabolism Lymphocyte Activation - drug effects Male Male genital diseases Medical sciences Microscopy, Fluorescence Middle Aged Nephrology. Urinary tract diseases Prostatic Hyperplasia - blood Prostatic Hyperplasia - metabolism Prostatic Hyperplasia - pathology Receptors, Androgen - metabolism Regular papers Testosterone - blood Testosterone - metabolism Transcription Factor RelA - metabolism Tumor Necrosis Factor-alpha - pharmacology Tumors Tumors of the urinary system Urinary tract. Prostate gland Vertebrates: endocrinology |
| title | Antiinflammatory effect of androgen receptor activation in human benign prostatic hyperplasia cells |
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