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Lactoferrin: Balancing Ups and Downs of Inflammation Due to Microbial Infections.

Authors :
Drago-Serrano, Maria Elisa
Campos-Rodríguez, Rafael
Carrero, Julio César
De La Garza, Mireya
Source :
International Journal of Molecular Sciences. Mar2017, Vol. 18 Issue 3, p501. 25p. 1 Diagram, 1 Chart.
Publication Year :
2017

Abstract

Lactoferrin (Lf) is a glycoprotein of the primary innate immune-defense system of mammals present in milk and other mucosal secretions. This protein of the transferrin family has broad antimicrobial properties by depriving pathogens from iron, or disrupting their plasma membranes through its highly cationic charge. Noteworthy, Lf also exhibits immunomodulatory activities performing up- and down-regulation of innate and adaptive immune cells, contributing to the homeostasis in mucosal surfaces exposed to myriad of microbial agents, such as the gastrointestinal and respiratory tracts. Although the inflammatory process is essential for the control of invasive infectious agents, the development of an exacerbated or chronic inflammation results in tissue damage with life-threatening consequences. In this review, we highlight recent findings in in vitro and in vivo models of the gut, lung, oral cavity, mammary gland, and liver infections that provide experimental evidence supporting the therapeutic role of human and bovine Lf in promoting some parameters of inflammation and protecting against the deleterious effects of bacterial, viral, fungal and protozoan-associated inflammation. Thus, this new knowledge of Lf immunomodulation paves the way to more effective design of treatments that include native or synthetic Lf derivatives, which may be useful to reduce immune-mediated tissue damage in infectious diseases. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
16616596
Volume :
18
Issue :
3
Database :
Academic Search Index
Journal :
International Journal of Molecular Sciences
Publication Type :
Academic Journal
Accession number :
122244006
Full Text :
https://doi.org/10.3390/ijms18030501