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Selenium and inflammation: underlying anti-inflammatory mechanisms.
Horm Metab Res 2009; 41(6):443-7HM

Abstract

The essential trace element selenium (Se), in the form of selenoproteins, plays a pivotal role in the antioxidant defense system of the cell. There is evidence that Se may confer benefits in patients with inflammatory disease and even infectious diseases like HIV. Furthermore, in patients with severe sepsis, characterized by an increase in reactive oxygen species and low endogenous anti-oxidative capacity, as well as in patients with systemic inflammatory response syndrome, Se supplementation may reduce mortality and improve the clinical outcome, respectively. The nuclear factor kappa-B (NF-kappaB) signaling pathway has been associated with enhanced inflammatory response and its activation has been significantly correlated with interleukin-6 and TNF-alpha production. Selenium may inhibit the activation of NF-kappaB by modulating selenoprotein genes expression. Moreover, Se supplementation in chronic inflammation restores the depleted hepatic and serum Se levels by increasing selenoprotein biosynthesis leading to suppressed CRP production thereby attenuating the inflammatory process. Se increases shedding of L-selectin from monocytes while decreasing soluble L-selectin, which has been reported to be associated with high mortality in patients with sepsis. These mechanisms are likely to contribute to the modulatory effects of an increased Se status on the inflammatory response. This review evaluates some apparently key mechanisms of the anti-inflammatory action of selenium and advocates Se supplementation as a modulator of inflammatory response in infectious and autoimmune disease. Prospective, randomized, controlled studies must be performed to provide a greater degree of certainty.

Authors+Show Affiliations

Endocrine Unit, Evgenidion Hospital, University of Athens Medical School, Athens, Greece. ledunt@otenet.gr

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

19418416

Citation

Duntas, L H.. "Selenium and Inflammation: Underlying Anti-inflammatory Mechanisms." Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme, vol. 41, no. 6, 2009, pp. 443-7.
Duntas LH. Selenium and inflammation: underlying anti-inflammatory mechanisms. Horm Metab Res. 2009;41(6):443-7.
Duntas, L. H. (2009). Selenium and inflammation: underlying anti-inflammatory mechanisms. Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme, 41(6), pp. 443-7. doi:10.1055/s-0029-1220724.
Duntas LH. Selenium and Inflammation: Underlying Anti-inflammatory Mechanisms. Horm Metab Res. 2009;41(6):443-7. PubMed PMID: 19418416.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selenium and inflammation: underlying anti-inflammatory mechanisms. A1 - Duntas,L H, Y1 - 2009/05/05/ PY - 2009/5/7/entrez PY - 2009/5/7/pubmed PY - 2009/8/7/medline SP - 443 EP - 7 JF - Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme JO - Horm. Metab. Res. VL - 41 IS - 6 N2 - The essential trace element selenium (Se), in the form of selenoproteins, plays a pivotal role in the antioxidant defense system of the cell. There is evidence that Se may confer benefits in patients with inflammatory disease and even infectious diseases like HIV. Furthermore, in patients with severe sepsis, characterized by an increase in reactive oxygen species and low endogenous anti-oxidative capacity, as well as in patients with systemic inflammatory response syndrome, Se supplementation may reduce mortality and improve the clinical outcome, respectively. The nuclear factor kappa-B (NF-kappaB) signaling pathway has been associated with enhanced inflammatory response and its activation has been significantly correlated with interleukin-6 and TNF-alpha production. Selenium may inhibit the activation of NF-kappaB by modulating selenoprotein genes expression. Moreover, Se supplementation in chronic inflammation restores the depleted hepatic and serum Se levels by increasing selenoprotein biosynthesis leading to suppressed CRP production thereby attenuating the inflammatory process. Se increases shedding of L-selectin from monocytes while decreasing soluble L-selectin, which has been reported to be associated with high mortality in patients with sepsis. These mechanisms are likely to contribute to the modulatory effects of an increased Se status on the inflammatory response. This review evaluates some apparently key mechanisms of the anti-inflammatory action of selenium and advocates Se supplementation as a modulator of inflammatory response in infectious and autoimmune disease. Prospective, randomized, controlled studies must be performed to provide a greater degree of certainty. SN - 1439-4286 UR - https://www.unboundmedicine.com/medline/citation/19418416/Selenium_and_inflammation:_underlying_anti_inflammatory_mechanisms_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1055/s-0029-1220724 DB - PRIME DP - Unbound Medicine ER -