Article Publish Status: FREE
Abstract Title:

Viral Hepatitis and Iron Dysregulation: Molecular Pathways and the Role of Lactoferrin.

Abstract Source:

Molecules. 2020 Apr 24 ;25(8). Epub 2020 Apr 24. PMID: 32344579

Abstract Author(s):

Romina Mancinelli, Luigi Rosa, Antimo Cutone, Maria Stefania Lepanto, Antonio Franchitto, Paolo Onori, Eugenio Gaudio, Piera Valenti

Article Affiliation:

Romina Mancinelli


The liver is a frontline immune site specifically designed to check and detect potential pathogens from the bloodstream to maintain a general state of immune hyporesponsiveness. One of the main functions of the liver is the regulation of iron homeostasis. The liver detects changes in systemic iron requirements and can regulate its concentration. Pathological states lead to the dysregulation of iron homeostasis which, in turn, can promote infectious and inflammatory processes. In this context, hepatic viruses deviate hepatocytes' iron metabolism in order to better replicate. Indeed, some viruses are able to alter the expression of iron-related proteins or exploit host receptors to enter inside host cells. Lactoferrin (Lf), a multifunctional iron-binding glycoprotein belonging to the innate immunity, is endowed with potent antiviral activity, mainly related to its ability to block viral entry into host cells by interacting with viral and/or cell surface receptors. Moreover, Lf can act as an iron scavenger by both direct iron-chelation or the modulation of the main iron-related proteins. In this review, the complex interplay between viral hepatitis, iron homeostasis, and inflammation as well as the role of Lf are outlined.

Study Type : Review
Additional Links
Pharmacological Actions : Antiviral Agents : CK(1957) : AC(1034)

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