Lactoferrin: Role in iron homeostasis and host defense against microbial infection
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The transferrin family of non-heme iron binding glycoproteins are believed to play a central role in iron metabolism and have been implicated in iron transport, cellular iron delivery and control of the level of free iron in external secretions. Lactoferrin (LF) is a member of this family that is widely localized in external fluids including milk and mucosal secretions, in addition to being a prominent component of the secondary granules of neutrophils. Although structurally related to transferrin, LF appears to have a broader functional role mediated by both iron dependent and iron independent mechanisms. In this review, we will focus on our current understanding on the role of LF in regulating iron homeostasis and its role in host protection against microbial infection at the mucosal surface. In addition, recent insights obtained from analyzing the phenotypic consequences of LF ablation in lactoferrin knockout mice (LFKO), which challenge the long held dogma that LF is required for intestinal iron absorption in the neonate, are summarized.
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- Brock JH. 2002 The physiology of lactoferrin. Biochem Cell Biol 80, 1-6.Google Scholar
- Ganz T. 2003 Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation. Blood.Google Scholar
- Longhi C, Conte MP, Seganti L et al. 1993 Influence of lactoferrin on the entry process of Escherichia coli HB101 (pRI203) in HeLa cells. Med Microbiol Immunol (Berl) 182, 25-35.Google Scholar
- Masson PL, Heremans JF, Schonne E. 1969 Lactoferrin, an ironbinding protein in neutrophilic leukocytes. J ExpMed 130, 643-658.Google Scholar
- Masson PL, Heremans, JF, Dive C. 1966 An iron-binding protein common to many external secretions. Clinica Chimica Acta 14, 735-739.Google Scholar
- Schaible UE, Collins HL, Priem F, Kaufmann SH. 2002 Correction of the iron overload defect in beta-2-microglobulin knockout mice by lactoferrin abolishes their increased susceptibility to tuberculosis. J ExpMed 196, 1507-1513.Google Scholar