Helminth- and Bacillus Calmette-Guérin-induced immunity in children sensitized in utero to filariasis and schistosomiasis.
Identifieur interne : 004C65 ( PubMed/Corpus ); précédent : 004C64; suivant : 004C66Helminth- and Bacillus Calmette-Guérin-induced immunity in children sensitized in utero to filariasis and schistosomiasis.
Auteurs : I. Malhotra ; P. Mungai ; A. Wamachi ; J. Kioko ; J H Ouma ; J W Kazura ; C L KingSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 1999.
English descriptors
- KwdEn :
- Adolescent, Adult, Animals, Antigens, Helminth (immunology), Cells, Cultured, Child, Child, Preschool, Cross-Sectional Studies, Cytokines (biosynthesis), Elephantiasis, Filarial (epidemiology), Elephantiasis, Filarial (immunology), Epitopes, T-Lymphocyte (immunology), Female, Humans, Immunity, Maternally-Acquired (immunology), Infant, Infant, Newborn, Kenya (epidemiology), Leukocytes, Mononuclear (metabolism), Male, Maternal-Fetal Exchange (immunology), Mycobacterium bovis (immunology), Pregnancy, Prospective Studies, Schistosoma haematobium (immunology), Schistosomiasis haematobia (epidemiology), Schistosomiasis haematobia (immunology), Tuberculin (immunology), Wuchereria bancrofti (immunology).
- MESH :
- chemical , biosynthesis : Cytokines.
- chemical , immunology : Antigens, Helminth, Epitopes, T-Lymphocyte, Tuberculin.
- geographic , epidemiology : Kenya.
- epidemiology : Elephantiasis, Filarial, Schistosomiasis haematobia.
- immunology : Elephantiasis, Filarial, Immunity, Maternally-Acquired, Maternal-Fetal Exchange, Mycobacterium bovis, Schistosoma haematobium, Schistosomiasis haematobia, Wuchereria bancrofti.
- metabolism : Leukocytes, Mononuclear.
- Adolescent, Adult, Animals, Cells, Cultured, Child, Child, Preschool, Cross-Sectional Studies, Female, Humans, Infant, Infant, Newborn, Male, Pregnancy, Prospective Studies.
Abstract
Infants and children are routinely vaccinated with bacillus Calmette-Guérin (BCG) in areas of the world where worm infections are common. Because maternal helminth infection during pregnancy can sensitize the developing fetus, we studied whether this prenatal immunity persists in childhood and modifies the immune response to BCG. Children and newborns living in rural Kenya, where BCG is administered at birth and filariasis and schistosomiasis are endemic, were examined. T cells from 2- to 10-year-old children of mothers without filariasis or schistosomiasis produced 10-fold more IFN-gamma in response to mycobacterial purified protein derivative than children of helminth-infected mothers (p < 0.01). This relationship was restricted to purified protein derivative because maternal infection status did not correlate with filarial Ag-driven IL-2, IFN-gamma, IL-4, or IL-5 responses by children. Prospective studies initiated at birth showed that helminth-specific T cell immunity acquired in utero is maintained until at least 10-14 mo of age in the absence of infection with either Wuchereria bancrofti or Schistosoma haematobium. Purified protein derivative-driven T cell IFN-gamma production evaluated 10-14 mo after BCG vaccination was 26-fold higher for infants who were not sensitized to filariae or schistosomes in utero relative to subjects who experienced prenatal sensitization (p < 0.01). These data indicate that helminth-specific immune responses acquired during gestation persist into childhood and that this prenatal sensitization biases T cell immunity induced by BCG vaccination away from type 1 IFN-gamma responses associated with protection against mycobacterial infection.
PubMed: 10352306
Links to Exploration step
pubmed:10352306Le document en format XML
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<author><name sortKey="Malhotra, I" sort="Malhotra, I" uniqKey="Malhotra I" first="I" last="Malhotra">I. Malhotra</name>
<affiliation><nlm:affiliation>Division of Geographic Medicine, Case Western Reserve University School of Medicine, University Hospitals of Cleveland, OH 44106, USA.</nlm:affiliation>
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<author><name sortKey="Mungai, P" sort="Mungai, P" uniqKey="Mungai P" first="P" last="Mungai">P. Mungai</name>
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<author><name sortKey="Wamachi, A" sort="Wamachi, A" uniqKey="Wamachi A" first="A" last="Wamachi">A. Wamachi</name>
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<author><name sortKey="Kioko, J" sort="Kioko, J" uniqKey="Kioko J" first="J" last="Kioko">J. Kioko</name>
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<author><name sortKey="Ouma, J H" sort="Ouma, J H" uniqKey="Ouma J" first="J H" last="Ouma">J H Ouma</name>
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<author><name sortKey="Mungai, P" sort="Mungai, P" uniqKey="Mungai P" first="P" last="Mungai">P. Mungai</name>
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<author><name sortKey="Ouma, J H" sort="Ouma, J H" uniqKey="Ouma J" first="J H" last="Ouma">J H Ouma</name>
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<author><name sortKey="Kazura, J W" sort="Kazura, J W" uniqKey="Kazura J" first="J W" last="Kazura">J W Kazura</name>
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<term>Adult</term>
<term>Animals</term>
<term>Antigens, Helminth (immunology)</term>
<term>Cells, Cultured</term>
<term>Child</term>
<term>Child, Preschool</term>
<term>Cross-Sectional Studies</term>
<term>Cytokines (biosynthesis)</term>
<term>Elephantiasis, Filarial (epidemiology)</term>
<term>Elephantiasis, Filarial (immunology)</term>
<term>Epitopes, T-Lymphocyte (immunology)</term>
<term>Female</term>
<term>Humans</term>
<term>Immunity, Maternally-Acquired (immunology)</term>
<term>Infant</term>
<term>Infant, Newborn</term>
<term>Kenya (epidemiology)</term>
<term>Leukocytes, Mononuclear (metabolism)</term>
<term>Male</term>
<term>Maternal-Fetal Exchange (immunology)</term>
<term>Mycobacterium bovis (immunology)</term>
<term>Pregnancy</term>
<term>Prospective Studies</term>
<term>Schistosoma haematobium (immunology)</term>
<term>Schistosomiasis haematobia (epidemiology)</term>
<term>Schistosomiasis haematobia (immunology)</term>
<term>Tuberculin (immunology)</term>
<term>Wuchereria bancrofti (immunology)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antigens, Helminth</term>
<term>Epitopes, T-Lymphocyte</term>
<term>Tuberculin</term>
</keywords>
<keywords scheme="MESH" type="geographic" qualifier="epidemiology" xml:lang="en"><term>Kenya</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Elephantiasis, Filarial</term>
<term>Schistosomiasis haematobia</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Elephantiasis, Filarial</term>
<term>Immunity, Maternally-Acquired</term>
<term>Maternal-Fetal Exchange</term>
<term>Mycobacterium bovis</term>
<term>Schistosoma haematobium</term>
<term>Schistosomiasis haematobia</term>
<term>Wuchereria bancrofti</term>
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<term>Animals</term>
<term>Cells, Cultured</term>
<term>Child</term>
<term>Child, Preschool</term>
<term>Cross-Sectional Studies</term>
<term>Female</term>
<term>Humans</term>
<term>Infant</term>
<term>Infant, Newborn</term>
<term>Male</term>
<term>Pregnancy</term>
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<front><div type="abstract" xml:lang="en">Infants and children are routinely vaccinated with bacillus Calmette-Guérin (BCG) in areas of the world where worm infections are common. Because maternal helminth infection during pregnancy can sensitize the developing fetus, we studied whether this prenatal immunity persists in childhood and modifies the immune response to BCG. Children and newborns living in rural Kenya, where BCG is administered at birth and filariasis and schistosomiasis are endemic, were examined. T cells from 2- to 10-year-old children of mothers without filariasis or schistosomiasis produced 10-fold more IFN-gamma in response to mycobacterial purified protein derivative than children of helminth-infected mothers (p < 0.01). This relationship was restricted to purified protein derivative because maternal infection status did not correlate with filarial Ag-driven IL-2, IFN-gamma, IL-4, or IL-5 responses by children. Prospective studies initiated at birth showed that helminth-specific T cell immunity acquired in utero is maintained until at least 10-14 mo of age in the absence of infection with either Wuchereria bancrofti or Schistosoma haematobium. Purified protein derivative-driven T cell IFN-gamma production evaluated 10-14 mo after BCG vaccination was 26-fold higher for infants who were not sensitized to filariae or schistosomes in utero relative to subjects who experienced prenatal sensitization (p < 0.01). These data indicate that helminth-specific immune responses acquired during gestation persist into childhood and that this prenatal sensitization biases T cell immunity induced by BCG vaccination away from type 1 IFN-gamma responses associated with protection against mycobacterial infection.</div>
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<Abstract><AbstractText>Infants and children are routinely vaccinated with bacillus Calmette-Guérin (BCG) in areas of the world where worm infections are common. Because maternal helminth infection during pregnancy can sensitize the developing fetus, we studied whether this prenatal immunity persists in childhood and modifies the immune response to BCG. Children and newborns living in rural Kenya, where BCG is administered at birth and filariasis and schistosomiasis are endemic, were examined. T cells from 2- to 10-year-old children of mothers without filariasis or schistosomiasis produced 10-fold more IFN-gamma in response to mycobacterial purified protein derivative than children of helminth-infected mothers (p < 0.01). This relationship was restricted to purified protein derivative because maternal infection status did not correlate with filarial Ag-driven IL-2, IFN-gamma, IL-4, or IL-5 responses by children. Prospective studies initiated at birth showed that helminth-specific T cell immunity acquired in utero is maintained until at least 10-14 mo of age in the absence of infection with either Wuchereria bancrofti or Schistosoma haematobium. Purified protein derivative-driven T cell IFN-gamma production evaluated 10-14 mo after BCG vaccination was 26-fold higher for infants who were not sensitized to filariae or schistosomes in utero relative to subjects who experienced prenatal sensitization (p < 0.01). These data indicate that helminth-specific immune responses acquired during gestation persist into childhood and that this prenatal sensitization biases T cell immunity induced by BCG vaccination away from type 1 IFN-gamma responses associated with protection against mycobacterial infection.</AbstractText>
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