Abstract
Lipocalin is a family of small molecules transporting extracellular proteins. Lipocalin-2 (LCN2) is a member of the family that sequesters iron-bound bacterial siderophores. The well-accepted function of LCN2 protein is its anti-bacterial behavior, however, its role in iron regulation, cellular migration, death and morphology modulation have been speculated. Several reports have correlated the presence of LCN2 in the infected, injured and stressed brain, and its effect in neuronal and non-neuronal cell types in the central nervous system. This article reviews studies that demonstrated mechanisms and functions of LCN2 expression in inflammed brain (acute and chronic), particularly in non-pathogen-associated neuroinflammation. This review predicts that LCN2 can be an attractive target to reduce mortality and morbidity associated with uncontrollable neuroinflammation.
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