TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative Stress
Objective. “Oxinflammation” is a recently coined term that defines the deleterious crosstalk between inflammatory and redox systemic processes, which underlie several diseases. Oxinflammation could be latently responsible for the predisposition of certain healthy individuals to disease development....
Saved in:
| Main Authors: | , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2018-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2018/9629537 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832565711628664832 |
|---|---|
| author | Veronica Tisato Stefania Gallo Elisabetta Melloni Claudio Celeghini Angelina Passaro Giorgio Zauli Paola Secchiero Carlo Bergamini Alessandro Trentini Gloria Bonaccorsi Giuseppe Valacchi Giovanni Zuliani Carlo Cervellati |
| author_facet | Veronica Tisato Stefania Gallo Elisabetta Melloni Claudio Celeghini Angelina Passaro Giorgio Zauli Paola Secchiero Carlo Bergamini Alessandro Trentini Gloria Bonaccorsi Giuseppe Valacchi Giovanni Zuliani Carlo Cervellati |
| author_sort | Veronica Tisato |
| collection | DOAJ |
| description | Objective. “Oxinflammation” is a recently coined term that defines the deleterious crosstalk between inflammatory and redox systemic processes, which underlie several diseases. Oxinflammation could be latently responsible for the predisposition of certain healthy individuals to disease development. The oxinflammatory pathway has been recently suggested to play a crucial role in regulating the activity of TNF-related apoptosis-inducing ligand (TRAIL), a TNF superfamily member that can mediate multiple signals in physiological and pathological processes. Therefore, we investigated the associations between TRAIL and key players of vascular redox homeostasis. Methods. We measured circulating TRAIL levels relative to praoxonas-1, lipoprotein phospholipase-A2, and ceruloplasmin levels in a cohort of healthy subjects (n=209). Results. Multivariate analysis revealed that ceruloplasmin levels were significantly inversely associated with TRAIL levels (r=−0.431, p<0.001). The observed association retained statistical significance after adjustment for additional confounding factors. After stratification for high-sensitivity C-reactive protein levels, the inverse association between TRAIL and ceruloplasmin levels remained strong and significant (r=−0.508, p<0.001, R2=0.260) only in the presence of inflammation, confirming the role of inflammation as emerged in in vitro experiments where recombinant TRAIL decreased ceruloplasmin expression levels in TNF-treated PBMC cultures. Conclusion. The results indicated that in an inflammatory milieu, TRAIL downregulates ceruloplasmin expression, highlighting a signaling axis involving TRAIL and ceruloplasmin that are linked via inflammation and providing important insights with potential clinical implications. |
| format | Article |
| id | doaj-art-5574c15e37984cedb6a57fb31f65b16e |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-5574c15e37984cedb6a57fb31f65b16e2025-02-03T01:06:55ZengWileyMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/96295379629537TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative StressVeronica Tisato0Stefania Gallo1Elisabetta Melloni2Claudio Celeghini3Angelina Passaro4Giorgio Zauli5Paola Secchiero6Carlo Bergamini7Alessandro Trentini8Gloria Bonaccorsi9Giuseppe Valacchi10Giovanni Zuliani11Carlo Cervellati12Department of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, ItalyDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, ItalyDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, ItalyDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, ItalyDepartment of Medical Science, University of Ferrara, Ferrara, ItalyDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, ItalyDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, ItalyDepartment of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, ItalyDepartment of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, ItalyDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, ItalyDepartment of Life Sciences and Biotechnology, University of Ferrara, Ferrara, ItalyDepartment of Morphology, Surgery and Experimental Medicine and LTTA Centre, University of Ferrara, Ferrara, ItalyDepartment of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, ItalyObjective. “Oxinflammation” is a recently coined term that defines the deleterious crosstalk between inflammatory and redox systemic processes, which underlie several diseases. Oxinflammation could be latently responsible for the predisposition of certain healthy individuals to disease development. The oxinflammatory pathway has been recently suggested to play a crucial role in regulating the activity of TNF-related apoptosis-inducing ligand (TRAIL), a TNF superfamily member that can mediate multiple signals in physiological and pathological processes. Therefore, we investigated the associations between TRAIL and key players of vascular redox homeostasis. Methods. We measured circulating TRAIL levels relative to praoxonas-1, lipoprotein phospholipase-A2, and ceruloplasmin levels in a cohort of healthy subjects (n=209). Results. Multivariate analysis revealed that ceruloplasmin levels were significantly inversely associated with TRAIL levels (r=−0.431, p<0.001). The observed association retained statistical significance after adjustment for additional confounding factors. After stratification for high-sensitivity C-reactive protein levels, the inverse association between TRAIL and ceruloplasmin levels remained strong and significant (r=−0.508, p<0.001, R2=0.260) only in the presence of inflammation, confirming the role of inflammation as emerged in in vitro experiments where recombinant TRAIL decreased ceruloplasmin expression levels in TNF-treated PBMC cultures. Conclusion. The results indicated that in an inflammatory milieu, TRAIL downregulates ceruloplasmin expression, highlighting a signaling axis involving TRAIL and ceruloplasmin that are linked via inflammation and providing important insights with potential clinical implications.http://dx.doi.org/10.1155/2018/9629537 |
| spellingShingle | Veronica Tisato Stefania Gallo Elisabetta Melloni Claudio Celeghini Angelina Passaro Giorgio Zauli Paola Secchiero Carlo Bergamini Alessandro Trentini Gloria Bonaccorsi Giuseppe Valacchi Giovanni Zuliani Carlo Cervellati TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative Stress Mediators of Inflammation |
| title | TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative Stress |
| title_full | TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative Stress |
| title_fullStr | TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative Stress |
| title_full_unstemmed | TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative Stress |
| title_short | TRAIL and Ceruloplasmin Inverse Correlation as a Representative Crosstalk between Inflammation and Oxidative Stress |
| title_sort | trail and ceruloplasmin inverse correlation as a representative crosstalk between inflammation and oxidative stress |
| url | http://dx.doi.org/10.1155/2018/9629537 |
| work_keys_str_mv | AT veronicatisato trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT stefaniagallo trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT elisabettamelloni trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT claudioceleghini trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT angelinapassaro trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT giorgiozauli trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT paolasecchiero trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT carlobergamini trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT alessandrotrentini trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT gloriabonaccorsi trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT giuseppevalacchi trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT giovannizuliani trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress AT carlocervellati trailandceruloplasmininversecorrelationasarepresentativecrosstalkbetweeninflammationandoxidativestress |