Adaptive immune response in symptomatic and asymptomatic enteric protozoal infection: evidence for a determining role of parasite genetic heterogeneity in host immunity to human giardiasis.
Identifieur interne : 000167 ( Main/Exploration ); précédent : 000166; suivant : 000168Adaptive immune response in symptomatic and asymptomatic enteric protozoal infection: evidence for a determining role of parasite genetic heterogeneity in host immunity to human giardiasis.
Auteurs : Zahra Babaei [Iran] ; Najmeh Malihi [Iran] ; Naser Zia-Ali [Iran] ; Iraj Sharifi [Iran] ; Mohammad A. Mohammadi [Iran] ; Martin F. Kagnoff [États-Unis] ; Lars Eckmann [États-Unis] ; Steven M. Singer [États-Unis] ; Shahram Solaymani-Mohammadi [États-Unis]Source :
- Microbes and infection [ 1769-714X ] ; 2016.
Descripteurs français
- KwdFr :
- ADN des protozoaires (génétique), Adolescent (MeSH), Adulte (MeSH), Analyse de séquence d'ADN (MeSH), Animaux (MeSH), Cytokines (sang), Enfant (MeSH), Enfant d'âge préscolaire (MeSH), Femelle (MeSH), Fèces (parasitologie), Giardia lamblia (génétique), Giardia lamblia (immunologie), Giardiase (immunologie), Giardiase (parasitologie), Génotype (MeSH), Humains (MeSH), Hétérogénéité génétique (MeSH), Immunité acquise (MeSH), Jeune adulte (MeSH), Lymphocytes auxiliaires Th1 (immunologie), Lymphocytes auxiliaires Th2 (immunologie), Mâle (MeSH), Phylogenèse (MeSH), Réaction de polymérisation en chaîne (MeSH), Études transversales (MeSH).
- MESH :
- génétique : ADN des protozoaires, Giardia lamblia.
- immunologie : Giardia lamblia, Giardiase, Lymphocytes auxiliaires Th1, Lymphocytes auxiliaires Th2.
- parasitologie : Fèces, Giardiase.
- sang : Cytokines.
- Adolescent, Adulte, Analyse de séquence d'ADN, Animaux, Enfant, Enfant d'âge préscolaire, Femelle, Génotype, Humains, Hétérogénéité génétique, Immunité acquise, Jeune adulte, Mâle, Phylogenèse, Réaction de polymérisation en chaîne, Études transversales.
English descriptors
- KwdEn :
- Adaptive Immunity (MeSH), Adolescent (MeSH), Adult (MeSH), Animals (MeSH), Child (MeSH), Child, Preschool (MeSH), Cross-Sectional Studies (MeSH), Cytokines (blood), DNA, Protozoan (genetics), Feces (parasitology), Female (MeSH), Genetic Heterogeneity (MeSH), Genotype (MeSH), Giardia lamblia (genetics), Giardia lamblia (immunology), Giardiasis (immunology), Giardiasis (parasitology), Humans (MeSH), Male (MeSH), Phylogeny (MeSH), Polymerase Chain Reaction (MeSH), Sequence Analysis, DNA (MeSH), Th1 Cells (immunology), Th2 Cells (immunology), Young Adult (MeSH).
- MESH :
- chemical , blood : Cytokines.
- chemical , genetics : DNA, Protozoan.
- genetics : Giardia lamblia.
- immunology : Giardia lamblia, Giardiasis, Th1 Cells, Th2 Cells.
- parasitology : Feces, Giardiasis.
- Adaptive Immunity, Adolescent, Adult, Animals, Child, Child, Preschool, Cross-Sectional Studies, Female, Genetic Heterogeneity, Genotype, Humans, Male, Phylogeny, Polymerase Chain Reaction, Sequence Analysis, DNA, Young Adult.
Abstract
The genetic basis of the ultimate clinical outcomes of human giardiasis has been the subject of numerous investigations. We previously demonstrated roles for both host and parasite factors in determining the outcome of enteric infection in a murine model of Giardia duodenalis infection. In the current study, fecal and serum specimens from healthy controls and human subjects infected with the intestinal parasite G. duodenalis were assessed. Using a semi-nested PCR method, clinical isolates were genetically characterized based on the gdh and tpi loci, and the phylogenetic trees were constructed. Using a sandwich ELISA method, the serum levels of representative TH1 and TH2 cytokines were measured in infected human subjects and healthy controls. Here we showed that symptomatic human giardiasis was characterized by significantly elevated serum levels of the TH1 cytokine IFN-γ compared to healthy controls, whereas asymptomatic human subjects and healthy controls had comparable levels of serum IFN-γ. Further analyses showed that human subjects infected with G. duodenalis genotype AI had significantly elevated levels of serum IFN-γ and IL-10, but not IL-5, whereas human subjects infected with AII had similar levels of those cytokines compared to healthy controls. These data demonstrate roles for both host and parasite factors in the determination of the outcome of enteric infections and may further broaden our understanding of host-parasite interaction during enteric protozoal infections.
DOI: 10.1016/j.micinf.2016.06.009
PubMed: 27401766
PubMed Central: PMC5071134
Affiliations:
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Mohammadi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman</wicri:regionArea><wicri:noRegion>Kerman</wicri:noRegion></affiliation></author><author><name sortKey="Kagnoff, Martin F" sort="Kagnoff, Martin F" uniqKey="Kagnoff M" first="Martin F" last="Kagnoff">Martin F. Kagnoff</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Eckmann, Lars" sort="Eckmann, Lars" uniqKey="Eckmann L" first="Lars" last="Eckmann">Lars Eckmann</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Singer, Steven M" sort="Singer, Steven M" uniqKey="Singer S" first="Steven M" last="Singer">Steven M. Singer</name><affiliation wicri:level="2"><nlm:affiliation>Department of Biology and Center for Infectious Disease, Georgetown University, Washington, DC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biology and Center for Infectious Disease, Georgetown University, Washington, DC</wicri:regionArea><placeName><region type="state">District de Columbia</region></placeName></affiliation></author><author><name sortKey="Solaymani Mohammadi, Shahram" sort="Solaymani Mohammadi, Shahram" uniqKey="Solaymani Mohammadi S" first="Shahram" last="Solaymani-Mohammadi">Shahram Solaymani-Mohammadi</name><affiliation wicri:level="2"><nlm:affiliation>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA, United States; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States. Electronic address: shahram.sm@nih.gov.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA, United States; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><series><title level="j">Microbes and infection</title><idno type="eISSN">1769-714X</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptive Immunity (MeSH)</term><term>Adolescent (MeSH)</term><term>Adult (MeSH)</term><term>Animals (MeSH)</term><term>Child (MeSH)</term><term>Child, Preschool (MeSH)</term><term>Cross-Sectional Studies (MeSH)</term><term>Cytokines (blood)</term><term>DNA, Protozoan (genetics)</term><term>Feces (parasitology)</term><term>Female (MeSH)</term><term>Genetic Heterogeneity (MeSH)</term><term>Genotype (MeSH)</term><term>Giardia lamblia (genetics)</term><term>Giardia lamblia (immunology)</term><term>Giardiasis (immunology)</term><term>Giardiasis (parasitology)</term><term>Humans (MeSH)</term><term>Male (MeSH)</term><term>Phylogeny (MeSH)</term><term>Polymerase Chain Reaction (MeSH)</term><term>Sequence Analysis, DNA (MeSH)</term><term>Th1 Cells (immunology)</term><term>Th2 Cells (immunology)</term><term>Young Adult (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN des protozoaires (génétique)</term><term>Adolescent (MeSH)</term><term>Adulte (MeSH)</term><term>Analyse de séquence d'ADN (MeSH)</term><term>Animaux (MeSH)</term><term>Cytokines (sang)</term><term>Enfant (MeSH)</term><term>Enfant d'âge préscolaire (MeSH)</term><term>Femelle (MeSH)</term><term>Fèces (parasitologie)</term><term>Giardia lamblia (génétique)</term><term>Giardia lamblia (immunologie)</term><term>Giardiase (immunologie)</term><term>Giardiase (parasitologie)</term><term>Génotype (MeSH)</term><term>Humains (MeSH)</term><term>Hétérogénéité génétique (MeSH)</term><term>Immunité acquise (MeSH)</term><term>Jeune adulte (MeSH)</term><term>Lymphocytes auxiliaires Th1 (immunologie)</term><term>Lymphocytes auxiliaires Th2 (immunologie)</term><term>Mâle (MeSH)</term><term>Phylogenèse (MeSH)</term><term>Réaction de polymérisation en chaîne (MeSH)</term><term>Études transversales (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>DNA, Protozoan</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Giardia lamblia</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ADN des protozoaires</term><term>Giardia lamblia</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Giardia lamblia</term><term>Giardiase</term><term>Lymphocytes auxiliaires Th1</term><term>Lymphocytes auxiliaires Th2</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Giardia lamblia</term><term>Giardiasis</term><term>Th1 Cells</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" qualifier="parasitologie" xml:lang="fr"><term>Fèces</term><term>Giardiase</term></keywords><keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Feces</term><term>Giardiasis</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Cytokines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adaptive Immunity</term><term>Adolescent</term><term>Adult</term><term>Animals</term><term>Child</term><term>Child, Preschool</term><term>Cross-Sectional Studies</term><term>Female</term><term>Genetic Heterogeneity</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Phylogeny</term><term>Polymerase Chain Reaction</term><term>Sequence Analysis, DNA</term><term>Young Adult</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adolescent</term><term>Adulte</term><term>Analyse de séquence d'ADN</term><term>Animaux</term><term>Enfant</term><term>Enfant d'âge préscolaire</term><term>Femelle</term><term>Génotype</term><term>Humains</term><term>Hétérogénéité génétique</term><term>Immunité acquise</term><term>Jeune adulte</term><term>Mâle</term><term>Phylogenèse</term><term>Réaction de polymérisation en chaîne</term><term>Études transversales</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The genetic basis of the ultimate clinical outcomes of human giardiasis has been the subject of numerous investigations. We previously demonstrated roles for both host and parasite factors in determining the outcome of enteric infection in a murine model of Giardia duodenalis infection. In the current study, fecal and serum specimens from healthy controls and human subjects infected with the intestinal parasite G. duodenalis were assessed. Using a semi-nested PCR method, clinical isolates were genetically characterized based on the gdh and tpi loci, and the phylogenetic trees were constructed. Using a sandwich ELISA method, the serum levels of representative T<sub>H1</sub> and T<sub>H2</sub> cytokines were measured in infected human subjects and healthy controls. Here we showed that symptomatic human giardiasis was characterized by significantly elevated serum levels of the T<sub>H1</sub> cytokine IFN-γ compared to healthy controls, whereas asymptomatic human subjects and healthy controls had comparable levels of serum IFN-γ. Further analyses showed that human subjects infected with G. duodenalis genotype AI had significantly elevated levels of serum IFN-γ and IL-10, but not IL-5, whereas human subjects infected with AII had similar levels of those cytokines compared to healthy controls. These data demonstrate roles for both host and parasite factors in the determination of the outcome of enteric infections and may further broaden our understanding of host-parasite interaction during enteric protozoal infections.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27401766</PMID><DateCompleted><Year>2017</Year><Month>05</Month><Day>03</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1769-714X</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><Issue>11</Issue><PubDate><Year>2016</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Microbes and infection</Title><ISOAbbreviation>Microbes Infect</ISOAbbreviation></Journal><ArticleTitle>Adaptive immune response in symptomatic and asymptomatic enteric protozoal infection: evidence for a determining role of parasite genetic heterogeneity in host immunity to human giardiasis.</ArticleTitle><Pagination><MedlinePgn>687-695</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S1286-4579(16)30092-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.micinf.2016.06.009</ELocationID><Abstract><AbstractText>The genetic basis of the ultimate clinical outcomes of human giardiasis has been the subject of numerous investigations. We previously demonstrated roles for both host and parasite factors in determining the outcome of enteric infection in a murine model of Giardia duodenalis infection. In the current study, fecal and serum specimens from healthy controls and human subjects infected with the intestinal parasite G. duodenalis were assessed. Using a semi-nested PCR method, clinical isolates were genetically characterized based on the gdh and tpi loci, and the phylogenetic trees were constructed. Using a sandwich ELISA method, the serum levels of representative T<sub>H1</sub> and T<sub>H2</sub> cytokines were measured in infected human subjects and healthy controls. Here we showed that symptomatic human giardiasis was characterized by significantly elevated serum levels of the T<sub>H1</sub> cytokine IFN-γ compared to healthy controls, whereas asymptomatic human subjects and healthy controls had comparable levels of serum IFN-γ. Further analyses showed that human subjects infected with G. duodenalis genotype AI had significantly elevated levels of serum IFN-γ and IL-10, but not IL-5, whereas human subjects infected with AII had similar levels of those cytokines compared to healthy controls. These data demonstrate roles for both host and parasite factors in the determination of the outcome of enteric infections and may further broaden our understanding of host-parasite interaction during enteric protozoal infections.</AbstractText><CopyrightInformation>Copyright © 2016 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Babaei</LastName><ForeName>Zahra</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran; Leishmaniasis Research Center, Kerman University of Medical Sciences, Kerman, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Malihi</LastName><ForeName>Najmeh</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zia-Ali</LastName><ForeName>Naser</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sharifi</LastName><ForeName>Iraj</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran; Leishmaniasis Research Center, Kerman University of Medical Sciences, Kerman, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mohammadi</LastName><ForeName>Mohammad A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Department of Medical Parasitology and Mycology, Kerman University of Medical Sciences, Kerman, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kagnoff</LastName><ForeName>Martin F</ForeName><Initials>MF</Initials><AffiliationInfo><Affiliation>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Eckmann</LastName><ForeName>Lars</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Singer</LastName><ForeName>Steven M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Department of Biology and Center for Infectious Disease, Georgetown University, Washington, DC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Solaymani-Mohammadi</LastName><ForeName>Shahram</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Mucosal Immunology, School of Medicine, University of California, La Jolla, CA, United States; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States. Electronic address: shahram.sm@nih.gov.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R15 AI109591</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AI112594</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D064888">Observational Study</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>07</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Microbes Infect</MedlineTA><NlmUniqueID>100883508</NlmUniqueID><ISSNLinking>1286-4579</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016054" MajorTopicYN="N">DNA, Protozoan</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005243" MajorTopicYN="N">Feces</DescriptorName><QualifierName UI="Q000469" MajorTopicYN="N">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018740" MajorTopicYN="Y">Genetic Heterogeneity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016829" MajorTopicYN="N">Giardia lamblia</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005873" MajorTopicYN="N">Giardiasis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000469" MajorTopicYN="Y">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010802" MajorTopicYN="N">Phylogeny</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016133" MajorTopicYN="N">Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017422" MajorTopicYN="N">Sequence Analysis, DNA</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018417" MajorTopicYN="N">Th1 Cells</DescriptorName><QualifierName UI="Q000276" 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Mohammadi</name><name sortKey="Sharifi, Iraj" sort="Sharifi, Iraj" uniqKey="Sharifi I" first="Iraj" last="Sharifi">Iraj Sharifi</name><name sortKey="Zia Ali, Naser" sort="Zia Ali, Naser" uniqKey="Zia Ali N" first="Naser" last="Zia-Ali">Naser Zia-Ali</name></country><country name="États-Unis"><region name="Californie"><name sortKey="Kagnoff, Martin F" sort="Kagnoff, Martin F" uniqKey="Kagnoff M" first="Martin F" last="Kagnoff">Martin F. Kagnoff</name></region><name sortKey="Eckmann, Lars" sort="Eckmann, Lars" uniqKey="Eckmann L" first="Lars" last="Eckmann">Lars Eckmann</name><name sortKey="Singer, Steven M" sort="Singer, Steven M" uniqKey="Singer S" first="Steven M" last="Singer">Steven M. Singer</name><name sortKey="Solaymani Mohammadi, Shahram" sort="Solaymani Mohammadi, Shahram" uniqKey="Solaymani Mohammadi S" first="Shahram" last="Solaymani-Mohammadi">Shahram Solaymani-Mohammadi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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