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Article ; Online: Crossing the Iron Gate: Why and How Transferrin Receptors Mediate Viral Entry.

Wessling-Resnick, Marianne

2018 Volume 38, Page(s) 431–458

Abstract: Because both the host and pathogen require iron, the innate immune response carefully orchestrates control over iron metabolism to limit its availability during times of infection. Nutritional iron deficiency can impair host immunity, while iron overload ...

Abstract	Because both the host and pathogen require iron, the innate immune response carefully orchestrates control over iron metabolism to limit its availability during times of infection. Nutritional iron deficiency can impair host immunity, while iron overload can cause oxidative stress to propagate harmful viral mutations. An emerging enigma is that many viruses use the primary gatekeeper of iron metabolism, the transferrin receptor, as a means to enter cells. Why and how this iron gate is a viral target for infection are the focus of this review.
MeSH term(s)	Animals ; Biological Transport ; Humans ; Immunity, Innate ; Iron/metabolism ; Receptors, Transferrin/metabolism ; Transferrin/metabolism ; Virus Internalization
Chemical Substances	Receptors, Transferrin ; Transferrin ; Iron (E1UOL152H7)
Language	English
Publishing date	2018-05-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	406980-8
ISSN	1545-4312 ; 0199-9885
ISSN (online)	1545-4312
ISSN	0199-9885
DOI	10.1146/annurev-nutr-082117-051749
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Article ; Online: Excess iron: considerations related to development and early growth.

Wessling-Resnick, Marianne

The American journal of clinical nutrition

2017 Volume 106, Issue Suppl 6, Page(s) 1600S–1605S

Abstract: What effects might arise from early life exposures to high iron? This review considers the specific effects of high iron on the brain, stem cells, and the process of erythropoiesis and identifies gaps in our knowledge of what molecular damage may be ... ...

Abstract	What effects might arise from early life exposures to high iron? This review considers the specific effects of high iron on the brain, stem cells, and the process of erythropoiesis and identifies gaps in our knowledge of what molecular damage may be incurred by oxidative stress that is imparted by high iron status in early life. Specific areas to enhance research on this topic include the following: longitudinal behavioral studies of children to test associations between iron exposures and mood, emotion, cognition, and memory; animal studies to determine epigenetic changes that reprogram brain development and metabolic changes in early life that could be followed through the life course; and the establishment of human epigenetic markers of iron exposures and oxidative stress that could be monitored for early origins of adult chronic diseases. In addition, efforts to understand how iron exposure influences stem cell biology could be enhanced by establishing platforms to collect biological specimens, including umbilical cord blood and amniotic fluid, to be made available to the research community. At the molecular level, there is a need to better understand stress erythropoiesis and changes in iron metabolism during pregnancy and development, especially with respect to regulatory control under high iron conditions that might promote ineffective erythropoiesis and iron-loading anemia. These investigations should focus not only on factors such as hepcidin and erythroferrone but should also include newly identified interactions between transferrin receptor-2 and the erythropoietin receptor. Finally, despite our understanding that several key micronutrients (e.g., vitamin A, copper, manganese, and zinc) support iron's function in erythropoiesis, how these nutrients interact remains, to our knowledge, unknown. It is necessary to consider many factors when formulating recommendations on iron supplementation.
MeSH term(s)	Brain/drug effects ; Brain/physiology ; Child Development/drug effects ; Erythropoiesis/drug effects ; Humans ; Infant ; Iron/administration & dosage ; Iron/blood ; Iron/toxicity ; Iron Overload/blood ; Stem Cells/drug effects
Chemical Substances	Iron (E1UOL152H7)
Language	English
Publishing date	2017-10-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	280048-2
ISSN	1938-3207 ; 0002-9165
ISSN (online)	1938-3207
ISSN	0002-9165
DOI	10.3945/ajcn.117.155879
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Article ; Online: Iron potentiates microglial interleukin-1β secretion induced by amyloid-β.

Nnah, Israel C / Lee, Chih-Hao / Wessling-Resnick, Marianne

Journal of neurochemistry

2020 Volume 154, Issue 2, Page(s) 177–189

Abstract: Alzheimer's disease (AD) is characterized by accumulation of amyloid-beta (Aβ) senile plaques in patients' brain tissues. Elevated levels of interleukin-1beta (IL-1β) have been identified in cerebrospinal fluid of living AD patients and in animal models ... ...

Abstract	Alzheimer's disease (AD) is characterized by accumulation of amyloid-beta (Aβ) senile plaques in patients' brain tissues. Elevated levels of interleukin-1beta (IL-1β) have been identified in cerebrospinal fluid of living AD patients and in animal models of AD. Increased expression of IL-1β and iron accumulation have been identified in microglial cells that cluster around amyloid plaques in AD mouse models and post-mortem brain tissues of AD patients. The goals of this study were to determine the effects of Aβ on the secretion of IL-1β by microglial cells and whether iron status influences this pro-inflammatory signaling cue. Immortalized microglial (IMG) cells were incubated with Aβ with or without iron. qRT-PCR and western blot analyses showed that Aβ induces biosynthesis of IL-1β by IMG cells. IMG cells secrete the mature form of IL-1β in a caspase 1-dependent manner. Incubation with iron provoked a greater pro-inflammatory response. Inhibition of the iron transporter divalent metal transporter 1 protected IMG cells against Aβ-induced inflammation. Potentiation of Aβ-elicited IL-1β induction by iron was also antagonized by ROS inhibitors, supporting the model that divalent metal transporter 1-mediated iron loading and subsequent increase in ROS contribute to the inflammatory effects of Aβ in microglia. Immunoblotting and immunofluorescence microscopy indicate that iron enhances Aβ activation of NF-κB signaling to promote IL-1β synthesis. These results support the hypothesis that Aβ stimulates IL-1β expression by activating NF-κB signaling in microglia cells. Most importantly, iron appears to exacerbate the pro-inflammatory effects of Aβ to increase IL-1β levels.
MeSH term(s)	Amyloid beta-Peptides/metabolism ; Amyloid beta-Peptides/pharmacology ; Animals ; Cell Line ; Interleukin-1beta/biosynthesis ; Iron/metabolism ; Iron/pharmacology ; Mice ; Microglia/drug effects ; Microglia/metabolism
Chemical Substances	Amyloid beta-Peptides ; Interleukin-1beta ; Iron (E1UOL152H7)
Language	English
Publishing date	2020-01-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.14906
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Article ; Online: Nramp1 and Other Transporters Involved in Metal Withholding during Infection.

Wessling-Resnick, Marianne

The Journal of biological chemistry

2015 Volume 290, Issue 31, Page(s) 18984–18990

Abstract: During the course of infection, many natural defenses are set up along the boundaries of the host-pathogen interface. Key among these is the host response to withhold metals to restrict the growth of invading microbes. This simple act of nutritional ... ...

Abstract	During the course of infection, many natural defenses are set up along the boundaries of the host-pathogen interface. Key among these is the host response to withhold metals to restrict the growth of invading microbes. This simple act of nutritional warfare, starving the invader of an essential element, is an effective means of limiting infection. The physiology of metal withholding is often referred to as "nutritional immunity," and the mechanisms of metal transport that contribute to this host response are the focus of this review.
MeSH term(s)	Animals ; Bacterial Infections/immunology ; Bacterial Infections/metabolism ; Biological Transport ; Cation Transport Proteins/physiology ; Homeostasis ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Iron/metabolism ; Manganese/metabolism
Chemical Substances	Cation Transport Proteins ; natural resistance-associated macrophage protein 1 ; Manganese (42Z2K6ZL8P) ; Iron (E1UOL152H7)
Language	English
Publishing date	2015-06-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.R115.643973
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Article ; Online: ZIP14 is degraded in response to manganese exposure.

Thompson, Khristy J / Wessling-Resnick, Marianne

Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine

2019 Volume 32, Issue 6, Page(s) 829–843

Abstract: Manganese (Mn) is an essential element necessary for proper development and brain function. Circulating Mn levels are regulated by hepatobiliary clearance to limit toxic levels and prevent tissue deposition. To characterize mechanisms involved in ... ...

Abstract	Manganese (Mn) is an essential element necessary for proper development and brain function. Circulating Mn levels are regulated by hepatobiliary clearance to limit toxic levels and prevent tissue deposition. To characterize mechanisms involved in hepatocyte Mn uptake, polarized human HepaRG cells were used for this study. Western blot analysis and immunofluorescence microscopy showed the Mn transporter ZIP14 was expressed and localized to the basolateral surface of polarized HepaRG cells. HepaRG cells took up
MeSH term(s)	Cation Transport Proteins/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Humans ; Manganese/pharmacology ; Proteolysis/drug effects ; Temperature
Chemical Substances	Cation Transport Proteins ; SLC39A14 protein, human ; Manganese (42Z2K6ZL8P)
Language	English
Publishing date	2019-09-20
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1112688-7
ISSN	1572-8773 ; 0966-0844
ISSN (online)	1572-8773
ISSN	0966-0844
DOI	10.1007/s10534-019-00216-1
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Article: Excess iron: considerations related to development and early growth

Wessling-Resnick, Marianne

American journal of clinical nutrition. 2017 Dec. 01, v. 106, no. suppl_6

2017

Abstract	What effects might arise from early life exposures to high iron? This review considers the specific effects of high iron on the brain, stem cells, and the process of erythropoiesis and identifies gaps in our knowledge of what molecular damage may be incurred by oxidative stress that is imparted by high iron status in early life. Specific areas to enhance research on this topic include the following: longitudinal behavioral studies of children to test associations between iron exposures and mood, emotion, cognition, and memory; animal studies to determine epigenetic changes that reprogram brain development and metabolic changes in early life that could be followed through the life course; and the establishment of human epigenetic markers of iron exposures and oxidative stress that could be monitored for early origins of adult chronic diseases. In addition, efforts to understand how iron exposure influences stem cell biology could be enhanced by establishing platforms to collect biological specimens, including umbilical cord blood and amniotic fluid, to be made available to the research community. At the molecular level, there is a need to better understand stress erythropoiesis and changes in iron metabolism during pregnancy and development, especially with respect to regulatory control under high iron conditions that might promote ineffective erythropoiesis and iron-loading anemia. These investigations should focus not only on factors such as hepcidin and erythroferrone but should also include newly identified interactions between transferrin receptor-2 and the erythropoietin receptor. Finally, despite our understanding that several key micronutrients (e.g., vitamin A, copper, manganese, and zinc) support iron's function in erythropoiesis, how these nutrients interact remains, to our knowledge, unknown. It is necessary to consider many factors when formulating recommendations on iron supplementation.
Keywords	adults ; amniotic fluid ; anemia ; blood ; brain ; children ; chronic diseases ; cognition ; copper ; emotions ; epigenetics ; erythropoiesis ; erythropoietin ; hepcidin ; iron ; iron absorption ; manganese ; memory ; nutrients ; oxidative stress ; pregnancy ; stem cells ; transferrin ; umbilical cord ; vitamin A ; zinc
Language	English
Dates of publication	2017-1201
Size	p. 1600S-1605S.
Publishing place	Oxford University Press
Document type	Article
ZDB-ID	280048-2
ISSN	1938-3207 ; 0002-9165
ISSN (online)	1938-3207
ISSN	0002-9165
DOI	10.3945/ajcn.117.155879
Database	NAL-Catalogue (AGRICOLA)

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Article: Brain Iron Homeostasis: A Focus on Microglial Iron.

Nnah, Israel C / Wessling-Resnick, Marianne

Pharmaceuticals (Basel, Switzerland)

2018 Volume 11, Issue 4

Abstract: Iron is an essential trace element required for important brain functions including oxidative metabolism, synaptic plasticity, myelination, and the synthesis of neurotransmitters. Disruptions in brain iron homeostasis underlie many neurodegenerative ... ...

Abstract	Iron is an essential trace element required for important brain functions including oxidative metabolism, synaptic plasticity, myelination, and the synthesis of neurotransmitters. Disruptions in brain iron homeostasis underlie many neurodegenerative diseases. Increasing evidence suggests that accumulation of brain iron and chronic neuroinflammation, characterized by microglia activation and secretion of proinflammatory cytokines, are hallmarks of neurodegenerative disorders including Alzheimer' s disease. While substantial efforts have led to an increased understanding of iron metabolism and the role of microglial cells in neuroinflammation, important questions still remain unanswered. Whether or not increased brain iron augments the inflammatory responses of microglial cells, including the molecular cues that guide such responses, is still unclear. How these brain macrophages accumulate, store, and utilize intracellular iron to carry out their various functions under normal and disease conditions is incompletely understood. Here, we describe the known and emerging mechanisms involved in microglial cell iron transport and metabolism as well as inflammatory responses in the brain, with a focus on AD.
Language	English
Publishing date	2018-11-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph11040129
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Article: Influence of Iron Deficiency on Olfactory Behavior in Weanling Rats.

Ruvin Kumara, V M / Wessling-Resnick, Marianne

Journal of behavioral and brain science

2017 Volume 2, Issue 2

Abstract: Chronically high occupational exposure to airborne metals like iron can impair olfactory function, but little is known about how low iron status modifies olfactory behavior. To investigate the influence of body iron status, weanling rats were fed a diet ... ...

Abstract	Chronically high occupational exposure to airborne metals like iron can impair olfactory function, but little is known about how low iron status modifies olfactory behavior. To investigate the influence of body iron status, weanling rats were fed a diet with low iron content (4 - 7 ppm) to induce iron deficiency anemia and olfactory behavior was compared to control rats fed an isocaloric diet sufficient in iron (210 - 220 ppm). Iron-deficient rats had prolonged exploratory time for attractive odorants in behavioral olfactory habituation/dis-habituation tests, olfactory preference tests and olfactory sensitivity tests compared with control rats. No significant differences were observed for aversive odorants between the two groups. These findings suggest that iron-dependent functions may be involved in controlling and processing of olfactory signal transduction via self and lateral inhibition such that odorant signal remains stronger for longer times prolonging exploratory activity on attractive odorants in the behavioral tests. These findings establish that iron deficiency can modify olfactory behavior.
Language	English
Publishing date	2017-05-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2621495-7
ISSN	2160-5874 ; 2160-5866
ISSN (online)	2160-5874
ISSN	2160-5866
DOI	10.4236/jbbs.2012.22020
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Pathophysiology of the Belgrade rat.

Veuthey, Tania / Wessling-Resnick, Marianne

Frontiers in pharmacology

2014 Volume 5, Page(s) 82

Abstract: The Belgrade rat is an animal model of divalent metal transporter 1 (DMT1) deficiency. This strain originates from an X-irradiation experiment first reported in 1966. Since then, the Belgrade rat's pathophysiology has helped to reveal the importance of ... ...

Abstract	The Belgrade rat is an animal model of divalent metal transporter 1 (DMT1) deficiency. This strain originates from an X-irradiation experiment first reported in 1966. Since then, the Belgrade rat's pathophysiology has helped to reveal the importance of iron balance and the role of DMT1. This review discusses our current understanding of iron transport homeostasis and summarizes molecular details of DMT1 function. We describe how studies of the Belgrade rat have revealed key roles for DMT1 in iron distribution to red blood cells as well as duodenal iron absorption. The Belgrade rat's pathology has extended our knowledge of hepatic iron handling, pulmonary and olfactory iron transport as well as brain iron uptake and renal iron handling. For example, relationships between iron and manganese metabolism have been discerned since both are essential metals transported by DMT1. Pathophysiologic features of the Belgrade rat provide us with a unique and interesting animal model to understand iron homeostasis.
Language	English
Publishing date	2014-04-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2014.00082
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Iron and mechanisms of emotional behavior.

Kim, Jonghan / Wessling-Resnick, Marianne

The Journal of nutritional biochemistry

2014 Volume 25, Issue 11, Page(s) 1101–1107

Abstract: Iron is required for appropriate behavioral organization. Iron deficiency results in poor brain myelination and impaired monoamine metabolism. Glutamate and γ-aminobutyric acid homeostasis is modified by changes in brain iron status. Such changes produce ...

Abstract	Iron is required for appropriate behavioral organization. Iron deficiency results in poor brain myelination and impaired monoamine metabolism. Glutamate and γ-aminobutyric acid homeostasis is modified by changes in brain iron status. Such changes produce not only deficits in memory/learning capacity and motor skills, but also emotional and psychological problems. An accumulating body of evidence indicates that both energy metabolism and neurotransmitter homeostasis influence emotional behavior, and both functions are influenced by brain iron status. Like other neurobehavioral aspects, the influence of iron metabolism on mechanisms of emotional behavior is multifactorial: brain region-specific control of behavior, regulation of neurotransmitters and associated proteins, temporal and regional differences in iron requirements, oxidative stress responses to excess iron, sex differences in metabolism, and interactions between iron and other metals. To better understand the role that brain iron plays in emotional behavior and mental health, this review discusses the pathologies associated with anxiety and other emotional disorders with respect to body iron status.
MeSH term(s)	Animals ; Brain/metabolism ; Emotions ; Female ; Humans ; Iron/metabolism ; Male ; Oxidative Stress ; Sex Factors
Chemical Substances	Iron (E1UOL152H7)
Language	English
Publishing date	2014-08-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1014929-6
ISSN	1873-4847 ; 0955-2863
ISSN (online)	1873-4847
ISSN	0955-2863
DOI	10.1016/j.jnutbio.2014.07.003
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