Dataset Information

A novel murine model of maternal micronutrient deficiencies and its implications in enteric inflammatory host-microbe interactions in the offspring

ABSTRACT: Micronutrient deficiency (MND i.e., lack of vitamins and minerals) during pregnancy is a major public health concern. Historically, studies have considered micronutrients in isolation; however, MNDs rarely occur alone. Furthermore, the impact of co-occurring MNDs on public health, mainly in shaping mucosal colonization by pathobionts from Enterobacteriaceae family, remain undetermined due to lack of relevant animal models.

INSTRUMENT(S): Bruker Daltonics instrument model

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Colon

SUBMITTER: Jenny Moon

LAB HEAD: B. Brett Finlay

PROVIDER: PXD041389 | Pride | 2024-05-24

REPOSITORIES: pride

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Dataset's files

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			Action	DRS
	MaxQuant_1.6.17.0.zip	Other
	Ravi_01_C1_1_1531.d.1.dar	Other
	Ravi_02_C2_1_1532.d.1.dar	Other
	Ravi_03_C3_1_1533.d.1.dar	Other
	Ravi_04_C4_1_1534.d.1.dar	Other

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Publications

A Murine Model of Maternal Micronutrient Deficiencies and Gut Inflammatory Host-microbe Interactions in the Offspring.

Holani Ravi R Littlejohn Paula T PT Edwards Karlie K Petersen Charisse C Moon Kyung-Mee KM Stacey Richard G RG Bozorgmehr Tahereh T Gerbec Zachary J ZJ Serapio-Palacios Antonio A Krekhno Zakhar Z Donald Katherine K Foster Leonard J LJ Turvey Stuart E SE Finlay B Brett BB

Cellular and molecular gastroenterology and hepatology 20240201 5

<h4>Background & aims</h4>Micronutrient deficiency (MND) (ie, lack of vitamins and minerals) during pregnancy is a major public health concern. Historically, studies have considered micronutrients in isolation; however, MNDs rarely occur alone. The impact of co-occurring MNDs on public health, mainly in shaping mucosal colonization by pathobionts from the Enterobacteriaceae family, remains undetermined due to lack of relevant animal models.<h4>Methods</h4>To establish a maternal murine model of ...[more]

PMID: 38307490

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Project description:Micronutrient deficiencies and environmental exposures have been to known to adversely impact brain and nervous system functions in adults and children worldwide. However, few studies have examined the short and long-term impact of these risk factors on neurodevelopmental outcomes in children in low-income countries, where the effects are likely to be more pronounced due to limited resources for monitoring and insufficient regulations. Biological risk factors of relevance include micronutrient deficiencies such as zinc and exposure to heavy metals such as lead and mercury. Studies have suggested an association between neurodevelopmental impairment and micronutrient deficiency as well as exposure to a number of heavy metals and environmental toxins. Moreover, findings also suggest that risk factors for adverse developmental outcomes that are independently significant may have the potential for causing cumulative increases in adverse effects. In Sub-Saharan Africa, severe malaria is a leading risk factor for long-term neurocognitive impairment in children. Zinc deficiency or exposure to heavy metals could influence risk of severe malaria, modify the risk of neurocognitive impairment in children with severe malaria, or independently affect risk of neurocognitive impairment. Untargeted analyses for potential environmental exposures or metabolomic changes in children with cerebral malaria vs. without cognitive impairment or in children with higher vs. lower cognitive scores, could also identify new risk factors for neurodevelopmental impairment in Ugandan children with cerebral malaria.In our completed study in Kampala, we assessed neurologic and developmental impairment in children with cerebral malaria [CM] or severe malarial anemia [SMA], as compared to health community children from the same extended household as the children with CM or SMA. As an extension of this study, we are interested in determining levels of micronutrients such as zinc in the population, and in addition, determining exposure levels of heavy metals (lead, mercury, copper, manganese etc.) in samples collected from children with severe malaria and community controls. The primary hypotheses of this study is that nutrient deficiencies or exposure to heavy metals influence short and long term neurocognitive outcomes in healthy community children and in children with severe malaria, and that children with cerebral malaria have specific metabolomic changes that relate to long-term neurocognitive impairment. The specific aims of our study are:Aim 1: To determine levels of zinc, heavy metals, and biomarkers associated with inflammation in children presenting with different forms of severe malaria (SM) and in healthy community children (CC). The working hypothesis of this aim is that 1) children with SM will have lower zinc levels compared to CC; 2) children with SM will present with higher toxic metal exposure and higher levels of biomarkers associated with inflammation than CC.Aim 2: To investigate how micronutrient deficiency, toxic metal exposure and inflammatory biomarkers affect short and long term neurodevelopmental outcomes and growth in children with severe malaria and community children (CC).The working hypothesis of this aim is that the lower levels of zinc, and presence of toxic metals in high concentrations will independently contribute to worsening neurodevelopmental outcomes and worsening growth over time in children with severe malaria and in community children. An alternate hypothesis is that micronutrient deficiency, toxic metal exposure and inflammatory states may interact with each other and with severe malaria to produce greater neurodevelopmental impairment, i.e., that the contribution is not independent but interactive.Aim 3: To determine whether the CSF metabolome differs according to level of neurodevelopmental impairment in children with cerebral malaria. The working hypothesis of this aim is that neurodevelopmental impairment in children with cerebral malaria is associated with changes in the CSF metabolome.