Developmental Exposures to Arsenic: Pneumonia, Immunity, and Microbiomes (DEAPIM)
砷的发育暴露:肺炎、免疫和微生物组 (DEAPIM)
基本信息
- 批准号:10745882
- 负责人:
- 金额:$ 73.53万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-02-05 至 2025-12-31
- 项目状态:未结题
- 来源:
- 关键词:16S ribosomal RNA sequencingAccountingAffectAgeAirAnimal ModelAnimalsAntibody ResponseAntibody titer measurementArsenicB-Cell DevelopmentBangladeshBirthBone MarrowCD4 Positive T LymphocytesCD8-Positive T-LymphocytesCell surfaceCellsCessation of lifeChildChildhoodColorCommunitiesComplexDNA DamageDNA RepairDataDendritic CellsDevelopmentDoseEnvironmental PollutantsExposure toFlow CytometryFoodGenesGoalsGranzymeHealthHospitalizationHumanImmuneImmune systemImmunityImmunologic MarkersImmunology procedureImpairmentIncidenceInfectionLeadLengthLifeLinkLymphocyteMeasuresMediatingMemoryMetagenomicsMorbidity - disease rateMothersNasopharynxOutcomePathway interactionsPeripheral Blood Mononuclear CellPlayPneumococcal vaccinePneumoniaPredispositionPregnancyProductionProliferatingQuantitative Reverse Transcriptase PCRRegulatory T-LymphocyteResearchResistance to infectionRespiratory Tract InfectionsRiskRoleShotgunsSignal TransductionStreptococcus pneumoniaeT cell differentiationT-Cell ActivationT-Cell DevelopmentT-Cell ProliferationT-LymphocyteT-Lymphocyte SubsetsTestingThymus GlandTimeToxic effectVaccinationVaccinesadaptive immunitybacteriomebooster vaccinecohortcytokinedrinking waterearly life exposureeffector T cellepidemiology studyexposed human populationgenotoxicityglobal healthgut microbiomegut microbiotaimmune functionimmunoregulationin uterometagenomic sequencingmicrobialmicrobial communitymicrobiomemicrobiotamonocytemortalityperforinprenatal exposurerespiratoryresponsestem cellsvaccine efficacyvaccine response
项目摘要
ABSTRACT
Exposure of human populations to arsenic via drinking water, air, and food is associated with significant
morbidity and mortality. Along with impairments in immune function, an increased susceptibility to pneumonia
has been observed in children exposed to high levels of arsenic. Pneumonia is a major global health concern
accounting for 70% of pediatric hospitalizations in the US alone. Epidemiological studies indicate a decrease in
the efficacy of respiratory vaccines in arsenic-exposed children. While vaccine efficacy is largely dependent on
host immune function, recent evidence indicates that the gut microbiome may also play a role. However, the
interrelationship of immune function and the microbiome on vaccine response in arsenic-exposed children has
not been studied. It is likely that early exposures to arsenic compromise vaccines protecting against
Streptococcus pneumoniae, the most common bacterial cause of pneumonia. The Scientific Premise is that
Early life and in utero arsenic exposure in children leads to alterations in adaptive immunity via dysregulation of
lymphocyte development and function. The impairment in these immune cells is responsible for decreases in
protection from upper airway infections (such as S. pneumoniae) due to decreased vaccine PCV10 efficacy, as
measured by S. pneumoniae nasopharyngeal (NP) carriage and anti-PCV circulating antibody titers. We also
posit that arsenic disrupts the gut microbiome which may alter vaccine efficacy, due to altered adaptive T cell
development. In Aim 1, we test the hypothesis that arsenic exposure in utero and during early life in children
(1-2 year) leads to (a) impaired PCV10 antibody responses following a booster dose of PCV10, and (b)
influences the NP microbiota diversity and the S. pneumoniae carriage. We will measure PCV10 titers and NP
carriage using qRT-PCR and full length 16s rRNA sequencing. In Aim 2, we test the hypothesis that alterations
in immune function and development are associated with early life arsenic exposure, leading to compromised
host immunity. These measures include PBMC immune biomarkers and functional immune assays including:
a) cell surface markers (CSM = T, B, NK, monocyte/dendritic cells, memory effector T cells) and the Th cell
subsets (Th1, Th2, Th4, Th17, Treg) using 11-color flow cytometry; b) T cell proliferation; c) ex vivo cytokine
production. In Aim 3 we test the hypothesis that differences in functional gut microbial composition are
influenced by immune development and immune function. We will assess the gut bacterial microbiome by
shotgun metagenomics and correlations with; a) PCV10 titers and the pneumococcal carriage (Aim1) and b)
changes in immune markers/function (Aim 2). The study will be conducted among 400 children in Bangladesh
ages between 1 and 2 years. Mothers of the participating children are part of a birth cohort and are followed
throughout their pregnancy, and children are extremely well characterized for arsenic exposure in utero. These
studies will provide new evidence on altered PCV vaccine response and the importance of the gut microbiome
in adverse health outcomes associated with arsenic.
摘要
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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{{ truncateString('SARAH J BLOSSOM', 18)}}的其他基金
New Mexico Integrative Science Program Incorporating Research in Environmental Sciences (NM-INSPIRES)
新墨西哥州综合科学计划纳入环境科学研究(NM-INSPIRES)
- 批准号:
10689665 - 财政年份:2022
- 资助金额:
$ 73.53万 - 项目类别:
New Mexico Integrative Science Program Incorporating Research in Environmental Sciences (NM-INSPIRES)
新墨西哥州综合科学计划纳入环境科学研究(NM-INSPIRES)
- 批准号:
10393297 - 财政年份:2022
- 资助金额:
$ 73.53万 - 项目类别:
Epigenetic modulation of CD4+ T cell differentiation and autoimmunity by trichloroethylene
三氯乙烯对 CD4 T 细胞分化和自身免疫的表观遗传调节
- 批准号:
10392944 - 财政年份:2021
- 资助金额:
$ 73.53万 - 项目类别:
Developmental Exposures to Arsenic: Pneumonia, Immunity, and Microbiomes (DEAPIM)
砷的发育暴露:肺炎、免疫和微生物组 (DEAPIM)
- 批准号:
10369655 - 财政年份:2021
- 资助金额:
$ 73.53万 - 项目类别:
Epigenetic modulation of CD4+ T cell differentiation and autoimmunity by trichloroethylene
三氯乙烯对 CD4 T 细胞分化和自身免疫的表观遗传调节
- 批准号:
10115737 - 财政年份:2021
- 资助金额:
$ 73.53万 - 项目类别:
CD4+ T cell-mediated neurotoxicity with continuous trichloroethylene exposure
持续接触三氯乙烯导致 CD4 T 细胞介导的神经毒性
- 批准号:
8755026 - 财政年份:2014
- 资助金额:
$ 73.53万 - 项目类别:
CD4+ T cell-mediated neurotoxicity with continuous trichloroethylene exposure
持续接触三氯乙烯导致 CD4 T 细胞介导的神经毒性
- 批准号:
8926236 - 财政年份:2014
- 资助金额:
$ 73.53万 - 项目类别:
CD4+ T cell-mediated neurotoxicity with continuous trichloroethylene exposure
持续接触三氯乙烯导致 CD4 T 细胞介导的神经毒性
- 批准号:
9067639 - 财政年份:2014
- 资助金额:
$ 73.53万 - 项目类别:
Developmental programming of TCE induced autoimmune disease
TCE诱导的自身免疫性疾病的发育编程
- 批准号:
8927709 - 财政年份:2012
- 资助金额:
$ 73.53万 - 项目类别:
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