Intranasal Administration of Recombinant Influenza Vaccines in Chimeric Mouse Models to Study Mucosal Immunity.
Identifieur interne : 000067 ( PubMed/Checkpoint ); précédent : 000066; suivant : 000068Intranasal Administration of Recombinant Influenza Vaccines in Chimeric Mouse Models to Study Mucosal Immunity.
Auteurs : José Vicente Pérez-Gir N ; Sergio G Mez-Medina ; Anja Lüdtke ; Cesar Munoz-Fontela [Allemagne]Source :
- Journal of visualized experiments : JoVE [ 1940-087X ] ; 2015.
Descripteurs français
- KwdFr :
- Animaux, Cellules HEK293, Cellules dendritiques (immunologie), Chimère, Femelle, Humains, Immunité muqueuse (), Lymphocytes T (immunologie), Souris, Souris de lignée C57BL, Sous-type H1N1 du virus de la grippe A (immunologie), Sous-type H2N2 du virus de la grippe A (immunologie), Vaccins antigrippaux (administration et posologie), Vaccins antigrippaux (génétique), Vaccins antigrippaux (immunologie), Vaccins synthétiques (administration et posologie), Vaccins synthétiques (génétique), Vaccins synthétiques (immunologie).
- MESH :
- administration et posologie : Vaccins antigrippaux, Vaccins synthétiques.
- génétique : Vaccins antigrippaux, Vaccins synthétiques.
- immunologie : Cellules dendritiques, Lymphocytes T, Sous-type H1N1 du virus de la grippe A, Sous-type H2N2 du virus de la grippe A, Vaccins antigrippaux, Vaccins synthétiques.
- Animaux, Cellules HEK293, Chimère, Femelle, Humains, Immunité muqueuse, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Animals, Chimera, Dendritic Cells (immunology), Female, HEK293 Cells, Humans, Immunity, Mucosal (drug effects), Influenza A Virus, H1N1 Subtype (immunology), Influenza A Virus, H2N2 Subtype (immunology), Influenza Vaccines (administration & dosage), Influenza Vaccines (genetics), Influenza Vaccines (immunology), Mice, Mice, Inbred C57BL, T-Lymphocytes (immunology), Vaccines, Synthetic (administration & dosage), Vaccines, Synthetic (genetics), Vaccines, Synthetic (immunology).
- MESH :
- chemical , administration & dosage : Influenza Vaccines, Vaccines, Synthetic.
- drug effects : Immunity, Mucosal.
- chemical , genetics : Influenza Vaccines, Vaccines, Synthetic.
- immunology : Dendritic Cells, Influenza A Virus, H1N1 Subtype, Influenza A Virus, H2N2 Subtype, Influenza Vaccines, T-Lymphocytes, Vaccines, Synthetic.
- Animals, Chimera, Female, HEK293 Cells, Humans, Mice, Mice, Inbred C57BL.
Abstract
Vaccines are one of the greatest achievements of mankind, and have saved millions of lives over the last century. Paradoxically, little is known about the physiological mechanisms that mediate immune responses to vaccines perhaps due to the overall success of vaccination, which has reduced interest into the molecular and physiological mechanisms of vaccine immunity. However, several important human pathogens including influenza virus still pose a challenge for vaccination, and may benefit from immune-based strategies. Although influenza reverse genetics has been successfully applied to the generation of live-attenuated influenza vaccines (LAIVs), the addition of molecular tools in vaccine preparations such as tracer components to follow up the kinetics of vaccination in vivo, has not been addressed. In addition, the recent generation of mouse models that allow specific depletion of leukocytes during kinetic studies has opened a window of opportunity to understand the basic immune mechanisms underlying vaccine-elicited protection. Here, we describe how the combination of reverse genetics and chimeric mouse models may help to provide new insights into how vaccines work at physiological and molecular levels, using as example a recombinant, cold-adapted, live-attenuated influenza vaccine (LAIV). We utilized laboratory-generated LAIVs harboring cell tracers as well as competitive bone marrow chimeras (BMCs) to determine the early kinetics of vaccine immunity and the main physiological mechanisms responsible for the initiation of vaccine-specific adaptive immunity. In addition, we show how this technique may facilitate gene function studies in single animals during immune responses to vaccines. We propose that this technique can be applied to improve current prophylactic strategies against pathogens for which urgent medical countermeasures are needed, for example influenza, HIV, Plasmodium, and hemorrhagic fever viruses such as Ebola virus.
DOI: 10.3791/52803
PubMed: 26168339
Affiliations:
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Paradoxically, little is known about the physiological mechanisms that mediate immune responses to vaccines perhaps due to the overall success of vaccination, which has reduced interest into the molecular and physiological mechanisms of vaccine immunity. However, several important human pathogens including influenza virus still pose a challenge for vaccination, and may benefit from immune-based strategies. Although influenza reverse genetics has been successfully applied to the generation of live-attenuated influenza vaccines (LAIVs), the addition of molecular tools in vaccine preparations such as tracer components to follow up the kinetics of vaccination in vivo, has not been addressed. In addition, the recent generation of mouse models that allow specific depletion of leukocytes during kinetic studies has opened a window of opportunity to understand the basic immune mechanisms underlying vaccine-elicited protection. Here, we describe how the combination of reverse genetics and chimeric mouse models may help to provide new insights into how vaccines work at physiological and molecular levels, using as example a recombinant, cold-adapted, live-attenuated influenza vaccine (LAIV). We utilized laboratory-generated LAIVs harboring cell tracers as well as competitive bone marrow chimeras (BMCs) to determine the early kinetics of vaccine immunity and the main physiological mechanisms responsible for the initiation of vaccine-specific adaptive immunity. In addition, we show how this technique may facilitate gene function studies in single animals during immune responses to vaccines. We propose that this technique can be applied to improve current prophylactic strategies against pathogens for which urgent medical countermeasures are needed, for example influenza, HIV, Plasmodium, and hemorrhagic fever viruses such as Ebola virus. </div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26168339</PMID><DateCompleted><Year>2015</Year><Month>09</Month><Day>09</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1940-087X</ISSN><JournalIssue CitedMedium="Internet"><Issue>100</Issue><PubDate><Year>2015</Year><Month>Jun</Month><Day>25</Day></PubDate></JournalIssue><Title>Journal of visualized experiments : JoVE</Title><ISOAbbreviation>J Vis Exp</ISOAbbreviation></Journal><ArticleTitle>Intranasal Administration of Recombinant Influenza Vaccines in Chimeric Mouse Models to Study Mucosal Immunity.</ArticleTitle><Pagination><MedlinePgn>e52803</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3791/52803</ELocationID><Abstract><AbstractText>Vaccines are one of the greatest achievements of mankind, and have saved millions of lives over the last century. Paradoxically, little is known about the physiological mechanisms that mediate immune responses to vaccines perhaps due to the overall success of vaccination, which has reduced interest into the molecular and physiological mechanisms of vaccine immunity. However, several important human pathogens including influenza virus still pose a challenge for vaccination, and may benefit from immune-based strategies. Although influenza reverse genetics has been successfully applied to the generation of live-attenuated influenza vaccines (LAIVs), the addition of molecular tools in vaccine preparations such as tracer components to follow up the kinetics of vaccination in vivo, has not been addressed. In addition, the recent generation of mouse models that allow specific depletion of leukocytes during kinetic studies has opened a window of opportunity to understand the basic immune mechanisms underlying vaccine-elicited protection. Here, we describe how the combination of reverse genetics and chimeric mouse models may help to provide new insights into how vaccines work at physiological and molecular levels, using as example a recombinant, cold-adapted, live-attenuated influenza vaccine (LAIV). We utilized laboratory-generated LAIVs harboring cell tracers as well as competitive bone marrow chimeras (BMCs) to determine the early kinetics of vaccine immunity and the main physiological mechanisms responsible for the initiation of vaccine-specific adaptive immunity. In addition, we show how this technique may facilitate gene function studies in single animals during immune responses to vaccines. We propose that this technique can be applied to improve current prophylactic strategies against pathogens for which urgent medical countermeasures are needed, for example influenza, HIV, Plasmodium, and hemorrhagic fever viruses such as Ebola virus. </AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pérez-Girón</LastName><ForeName>José Vicente</ForeName><Initials>JV</Initials><AffiliationInfo><Affiliation>Laboratory of Emerging Viruses, Heinrich Pette Institute, Leibniz Institute for Experimental Virology.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gómez-Medina</LastName><ForeName>Sergio</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Emerging Viruses, Heinrich Pette Institute, Leibniz Institute for Experimental Virology.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lüdtke</LastName><ForeName>Anja</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Laboratory of Emerging Viruses, Heinrich Pette Institute, Leibniz Institute for Experimental Virology.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Munoz-Fontela</LastName><ForeName>Cesar</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Laboratory of Emerging Viruses, Heinrich Pette Institute, Leibniz Institute for Experimental Virology; cesar.munoz-fontela@hpi.uni-hamburg.de.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D059040">Video-Audio Media</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>06</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Vis Exp</MedlineTA><NlmUniqueID>101313252</NlmUniqueID><ISSNLinking>1940-087X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007252">Influenza Vaccines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014614">Vaccines, Synthetic</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002678" MajorTopicYN="N">Chimera</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003713" MajorTopicYN="N">Dendritic Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018928" MajorTopicYN="N">Immunity, Mucosal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053121" MajorTopicYN="N">Influenza A Virus, H2N2 Subtype</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007252" MajorTopicYN="N">Influenza Vaccines</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014614" MajorTopicYN="N">Vaccines, Synthetic</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>7</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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uniqKey="Ludtke A" first="Anja" last="Lüdtke">Anja Lüdtke</name><name sortKey="Perez Gir N, Jose Vicente" sort="Perez Gir N, Jose Vicente" uniqKey="Perez Gir N J" first="José Vicente" last="Pérez-Gir N">José Vicente Pérez-Gir N</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Munoz Fontela, Cesar" sort="Munoz Fontela, Cesar" uniqKey="Munoz Fontela C" first="Cesar" last="Munoz-Fontela">Cesar Munoz-Fontela</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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