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Int J Vitam Nutr Res. 2010 Oct;80(4-5):271-7. doi: 10.1024/0300-9831/a000034.

Impact of zinc metabolism on innate immune function in the setting of sepsis.

Author information

1
Dorothy M. Davis Heart and Lung Research Institute, and Department of Pharmacy, The Ohio State University, Columbus, OH, USA. Daren.Knoell@osumc.edu

Abstract

Individuals at highest risk of zinc deficiency (children, elderly, pregnant and lactating women, morbidly ill, alcoholics) have a higher risk of infection. Whereas the essential role of zinc in maintaining adaptive immunity is well recognized, much less is known regarding the innate immune system. We recently reported that zinc deficiency significantly increases mortality in an animal model of sepsis. In particular, zinc-deficient mice had a decreased capacity to clear bacteria and a concomitant increase in NF-kappaB-mediated signaling across multiple vital organs. This occurred in tandem with exaggeration of the acute phase and innate immune response. Strikingly, sepsis patients revealed similar findings in that lower plasma zinc levels were associated with more inflammation and increased severity of illness. Through these investigations we have consistently observed that SLC39 A8 (ZIP8) is unique, relative to other zinc transporters, in that its expression is significantly induced at the onset of infection. Moreover, induction of ZIP8-mediated zinc transport into innate immune cells is vital for proper immune function. Whether ZIP8 functions beyond the conventional role of a zinc transporter remains a work in progress, although new evidence has revealed that ZIP8 expression itself is regulated by NF-kappaB. Taken together, these findings indicate that zinc is vital for proper innate immune function and that hZIP8 is intricately involved in maintaining innate immune defense.

PMID:
21462110
PMCID:
PMC3279174
DOI:
10.1024/0300-9831/a000034
[Indexed for MEDLINE]
Free PMC Article
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