NDLI: Lipocalin 2 deficiency dysregulates iron homeostasis and exacerbates endotoxin-induced sepsis.

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Lipocalin 2 deficiency dysregulates iron homeostasis and exacerbates endotoxin-induced sepsis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Srinivasan, Gayathri Aitken, Jesse D. Vijay-Kumar, Matam Zhang, Benyue Carvalho, Frederic A. Jones, Dean P. Chassaing, Benoit Borregaard, Niels Shashidharamurthy, Rangaiah Gewirtz, Andrew T.
Description	Country affiliation: United States Author Affiliation: Srinivasan G ( Department of Biology, Center for Inflammation, Immunity, and Infection, Georgia State University, Atlanta, GA 30303, USA.)
Abstract	Various states of inflammation, including sepsis, are associated with hypoferremia, which limits iron availability to pathogens and reduces iron-mediated oxidative stress. Lipocalin 2 (Lcn2; siderocalin, 24p3) plays a central role in iron transport. Accordingly, Lcn2-deficient (Lcn2KO) mice exhibit elevated intracellular labile iron. In this study, we report that LPS induced systemic Lcn2 by 150-fold in wild-type mice at 24 h. Relative to wild-type littermates, Lcn2KO mice were markedly more sensitive to endotoxemia, exhibiting elevated indices of organ damage (transaminasemia, lactate dehydrogenase) and increased mortality. Such exacerbated endotoxemia was associated with substantially increased caspase-3 cleavage and concomitantly elevated immune cell apoptosis. Furthermore, cells from Lcn2KO mice were hyperresponsive to LPS ex vivo, exhibiting elevated cytokine secretion. Additionally, Lcn2KO mice exhibited delayed LPS-induced hypoferremia despite normal hepatic hepcidin expression and displayed decreased levels of the tissue redox state indicators cysteine and glutathione in liver and plasma. Desferroxamine, an iron chelator, significantly protects Lcn2KO mice from LPS-induced toxicity, including mortality, suggesting that Lcn2 may act as an antioxidant in vivo by regulating iron homeostasis. Thus, Lcn2-mediated regulation of labile iron protects the host against sepsis. Its small size and simple structure may make Lcn2 a deployable treatment for sepsis.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200892
Journal	The Journal of Immunology
Issue Number	4
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-08-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Acute-phase Proteins Metabolism Homeostasis Physiology Lipocalins Oncogene Proteins Sepsis Deficiency Immunology Animals Apoptosis Endotoxins Toxicity Enzyme-linked Immunosorbent Assay Flow Cytometry Immunoblotting Mice Mice, Knockout Reverse Transcriptase Polymerase Chain Reaction Chemically Induced Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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