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Article: Innate immunity and the evolution of resistance to an emerging infectious disease in a wild bird

TitleInnate immunity and the evolution of resistance to an emerging infectious disease in a wild bird
Authors
Keywordscell-mediated immunity
immunosuppression
microevolution
time-series microarray
Issue Date2012
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/MEC
Citation
Molecular Ecology, 2012, v. 21 n. 11, p. 2628-2639 How to Cite?
AbstractInnate immunity is expected to play a primary role in conferring resistance to novel infectious diseases, but few studies have attempted to examine its role in the evolution of resistance to emerging pathogens in wild vertebrate populations. Here, we used experimental infections and cDNA microarrays to examine whether changes in the innate and/or acquired immune responses likely accompanied the emergence of resistance in house finches (Carpodacus mexicanus) in the eastern United States subject to a recent outbreak of conjunctivitis-causing bacterium (Mycoplasma gallisepticum-MG). Three days following experimental infection with MG, we observed differences in the splenic transcriptional responses between house finches from eastern U.S. populations, with a 12-year history of MG exposure, versus western U.S. populations, with no history of exposure to MG. In particular, western birds down-regulated gene expression, while eastern finches showed no expression change relative to controls. Studies involving poultry have shown that MG can manipulate host immunity, and our observations suggest that pathogen manipulation occurred only in finches from the western populations, outside the range of MG. Fourteen days after infection, eastern finches, but not western finches, up-regulated genes associated with acquired immunity (cell-mediated immunity) relative to controls. These observations suggest population differences in the temporal course of the response to infection with MG and imply that innate immune processes were targets of selection in response to MG in the eastern U.S. population. © 2012 Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/180753
ISSN
2021 Impact Factor: 6.622
2020 SCImago Journal Rankings: 2.619
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBonneaud, Cen_US
dc.contributor.authorBalenger, SLen_US
dc.contributor.authorZhang, Jen_US
dc.contributor.authorEdwards, SVen_US
dc.contributor.authorHill, GEen_US
dc.date.accessioned2013-01-28T01:42:18Z-
dc.date.available2013-01-28T01:42:18Z-
dc.date.issued2012en_US
dc.identifier.citationMolecular Ecology, 2012, v. 21 n. 11, p. 2628-2639en_US
dc.identifier.issn0962-1083en_US
dc.identifier.urihttp://hdl.handle.net/10722/180753-
dc.description.abstractInnate immunity is expected to play a primary role in conferring resistance to novel infectious diseases, but few studies have attempted to examine its role in the evolution of resistance to emerging pathogens in wild vertebrate populations. Here, we used experimental infections and cDNA microarrays to examine whether changes in the innate and/or acquired immune responses likely accompanied the emergence of resistance in house finches (Carpodacus mexicanus) in the eastern United States subject to a recent outbreak of conjunctivitis-causing bacterium (Mycoplasma gallisepticum-MG). Three days following experimental infection with MG, we observed differences in the splenic transcriptional responses between house finches from eastern U.S. populations, with a 12-year history of MG exposure, versus western U.S. populations, with no history of exposure to MG. In particular, western birds down-regulated gene expression, while eastern finches showed no expression change relative to controls. Studies involving poultry have shown that MG can manipulate host immunity, and our observations suggest that pathogen manipulation occurred only in finches from the western populations, outside the range of MG. Fourteen days after infection, eastern finches, but not western finches, up-regulated genes associated with acquired immunity (cell-mediated immunity) relative to controls. These observations suggest population differences in the temporal course of the response to infection with MG and imply that innate immune processes were targets of selection in response to MG in the eastern U.S. population. © 2012 Blackwell Publishing Ltd.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/MECen_US
dc.relation.ispartofMolecular Ecologyen_US
dc.subjectcell-mediated immunity-
dc.subjectimmunosuppression-
dc.subjectmicroevolution-
dc.subjecttime-series microarray-
dc.subject.meshAnimalsen_US
dc.subject.meshAnimals, Wilden_US
dc.subject.meshBiological Evolutionen_US
dc.subject.meshBird Diseases - Microbiologyen_US
dc.subject.meshDisease Resistance - Genetics - Immunologyen_US
dc.subject.meshFinches - Genetics - Immunology - Microbiologyen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshImmunity, Innate - Geneticsen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMycoplasma Infections - Immunology - Veterinaryen_US
dc.subject.meshMycoplasma Gallisepticum - Pathogenicityen_US
dc.subject.meshOligonucleotide Array Sequence Analysisen_US
dc.subject.meshUnited Statesen_US
dc.titleInnate immunity and the evolution of resistance to an emerging infectious disease in a wild birden_US
dc.typeArticleen_US
dc.identifier.emailZhang, J: jzhang1@hku.hken_US
dc.identifier.authorityZhang, J=rp01713en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1365-294X.2012.05551.xen_US
dc.identifier.pmid22512302-
dc.identifier.scopuseid_2-s2.0-84861574328en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84861574328&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume21en_US
dc.identifier.issue11en_US
dc.identifier.spage2628en_US
dc.identifier.epage2639en_US
dc.identifier.isiWOS:000304389500009-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridBonneaud, C=6507932232en_US
dc.identifier.scopusauthoridBalenger, SL=6506097429en_US
dc.identifier.scopusauthoridZhang, J=22137260600en_US
dc.identifier.scopusauthoridEdwards, SV=7401520541en_US
dc.identifier.scopusauthoridHill, GE=35500077500en_US
dc.identifier.issnl0962-1083-

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