Mosquito infection responses to developing filarial worms.
Identifieur interne : 002B63 ( PubMed/Checkpoint ); précédent : 002B62; suivant : 002B64Mosquito infection responses to developing filarial worms.
Auteurs : Sara M. Erickson [États-Unis] ; Zhiyong Xi ; George F. Mayhew ; Jose L. Ramirez ; Matthew T. Aliota ; Bruce M. Christensen ; George DimopoulosSource :
- PLoS neglected tropical diseases [ 1935-2735 ] ; 2009.
Descripteurs français
- KwdFr :
- Aedes (génétique), Aedes (immunologie), Aedes (parasitologie), Analyse de profil d'expression de gènes, Animaux, Femelle, Filarioidea (croissance et développement), Filarioidea (physiologie), Filariose lymphatique (parasitologie), Filariose lymphatique (transmission), Gerbillinae, Humains, Mâle, Séquençage par oligonucléotides en batterie, Vecteurs insectes (génétique), Vecteurs insectes (immunologie), Vecteurs insectes (parasitologie).
- MESH :
- croissance et développement : Filarioidea.
- génétique : Aedes, Vecteurs insectes.
- immunologie : Aedes, Vecteurs insectes.
- parasitologie : Aedes, Filariose lymphatique, Vecteurs insectes.
- physiologie : Filarioidea.
- transmission : Analyse de profil d'expression de gènes, Animaux, Femelle, Filariose lymphatique, Gerbillinae, Humains, Mâle, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- Aedes (genetics), Aedes (immunology), Aedes (parasitology), Animals, Elephantiasis, Filarial (parasitology), Elephantiasis, Filarial (transmission), Female, Filarioidea (growth & development), Filarioidea (physiology), Gene Expression Profiling, Gerbillinae, Humans, Insect Vectors (genetics), Insect Vectors (immunology), Insect Vectors (parasitology), Male, Oligonucleotide Array Sequence Analysis.
- MESH :
- genetics : Aedes, Insect Vectors.
- growth & development : Filarioidea.
- immunology : Aedes, Insect Vectors.
- parasitology : Aedes, Elephantiasis, Filarial, Insect Vectors.
- physiology : Filarioidea.
- transmission : Elephantiasis, Filarial.
- Animals, Female, Gene Expression Profiling, Gerbillinae, Humans, Male, Oligonucleotide Array Sequence Analysis.
Abstract
Human lymphatic filariasis is a mosquito-vectored disease caused by the nematode parasites Wuchereria bancrofti, Brugia malayi and Brugia timori. These are relatively large roundworms that can cause considerable damage in compatible mosquito vectors. In order to assess how mosquitoes respond to infection in compatible mosquito-filarial worm associations, microarray analysis was used to evaluate transcriptome changes in Aedes aegypti at various times during B. malayi development. Changes in transcript abundance in response to the different stages of B. malayi infection were diverse. At the early stages of midgut and thoracic muscle cell penetration, a greater number of genes were repressed compared to those that were induced (20 vs. 8). The non-feeding, intracellular first-stage larvae elicited few differences, with 4 transcripts showing an increased and 9 a decreased abundance relative to controls. Several cecropin transcripts increased in abundance after parasites molted to second-stage larvae. However, the greatest number of transcripts changed in abundance after larvae molted to third-stage larvae and migrated to the head and proboscis (120 induced, 38 repressed), including a large number of putative, immunity-related genes (approximately 13% of genes with predicted functions). To test whether the innate immune system of mosquitoes was capable of modulating permissiveness to the parasite, we activated the Toll and Imd pathway controlled rel family transcription factors Rel1 and Rel2 (by RNA interference knockdown of the pathway's negative regulators Cactus and Caspar) during the early stages of infection with B. malayi. The activation of either of these immune signaling pathways, or knockdown of the Toll pathway, did not affect B. malayi in Ae. aegypti. The possibility of LF parasites evading mosquito immune responses during successful development is discussed.
DOI: 10.1371/journal.pntd.0000529
PubMed: 19823571
Affiliations:
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pubmed:19823571Le document en format XML
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These are relatively large roundworms that can cause considerable damage in compatible mosquito vectors. In order to assess how mosquitoes respond to infection in compatible mosquito-filarial worm associations, microarray analysis was used to evaluate transcriptome changes in Aedes aegypti at various times during B. malayi development. Changes in transcript abundance in response to the different stages of B. malayi infection were diverse. At the early stages of midgut and thoracic muscle cell penetration, a greater number of genes were repressed compared to those that were induced (20 vs. 8). The non-feeding, intracellular first-stage larvae elicited few differences, with 4 transcripts showing an increased and 9 a decreased abundance relative to controls. Several cecropin transcripts increased in abundance after parasites molted to second-stage larvae. However, the greatest number of transcripts changed in abundance after larvae molted to third-stage larvae and migrated to the head and proboscis (120 induced, 38 repressed), including a large number of putative, immunity-related genes (approximately 13% of genes with predicted functions). To test whether the innate immune system of mosquitoes was capable of modulating permissiveness to the parasite, we activated the Toll and Imd pathway controlled rel family transcription factors Rel1 and Rel2 (by RNA interference knockdown of the pathway's negative regulators Cactus and Caspar) during the early stages of infection with B. malayi. The activation of either of these immune signaling pathways, or knockdown of the Toll pathway, did not affect B. malayi in Ae. aegypti. The possibility of LF parasites evading mosquito immune responses during successful development is discussed.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19823571</PMID><DateCreated><Year>2009</Year><Month>10</Month><Day>13</Day></DateCreated><DateCompleted><Year>2009</Year><Month>12</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1935-2735</ISSN><JournalIssue CitedMedium="Internet"><Volume>3</Volume><Issue>10</Issue><PubDate><Year>2009</Year><Month>Oct</Month><Day>13</Day></PubDate></JournalIssue><Title>PLoS neglected tropical diseases</Title><ISOAbbreviation>PLoS Negl Trop Dis</ISOAbbreviation></Journal><ArticleTitle>Mosquito infection responses to developing filarial worms.</ArticleTitle><Pagination><MedlinePgn>e529</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pntd.0000529</ELocationID><Abstract><AbstractText>Human lymphatic filariasis is a mosquito-vectored disease caused by the nematode parasites Wuchereria bancrofti, Brugia malayi and Brugia timori. These are relatively large roundworms that can cause considerable damage in compatible mosquito vectors. In order to assess how mosquitoes respond to infection in compatible mosquito-filarial worm associations, microarray analysis was used to evaluate transcriptome changes in Aedes aegypti at various times during B. malayi development. Changes in transcript abundance in response to the different stages of B. malayi infection were diverse. At the early stages of midgut and thoracic muscle cell penetration, a greater number of genes were repressed compared to those that were induced (20 vs. 8). The non-feeding, intracellular first-stage larvae elicited few differences, with 4 transcripts showing an increased and 9 a decreased abundance relative to controls. Several cecropin transcripts increased in abundance after parasites molted to second-stage larvae. However, the greatest number of transcripts changed in abundance after larvae molted to third-stage larvae and migrated to the head and proboscis (120 induced, 38 repressed), including a large number of putative, immunity-related genes (approximately 13% of genes with predicted functions). To test whether the innate immune system of mosquitoes was capable of modulating permissiveness to the parasite, we activated the Toll and Imd pathway controlled rel family transcription factors Rel1 and Rel2 (by RNA interference knockdown of the pathway's negative regulators Cactus and Caspar) during the early stages of infection with B. malayi. The activation of either of these immune signaling pathways, or knockdown of the Toll pathway, did not affect B. malayi in Ae. aegypti. The possibility of LF parasites evading mosquito immune responses during successful development is discussed.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Erickson</LastName><ForeName>Sara M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, Wisconsin, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xi</LastName><ForeName>Zhiyong</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Mayhew</LastName><ForeName>George F</ForeName><Initials>GF</Initials></Author><Author ValidYN="Y"><LastName>Ramirez</LastName><ForeName>Jose L</ForeName><Initials>JL</Initials></Author><Author ValidYN="Y"><LastName>Aliota</LastName><ForeName>Matthew T</ForeName><Initials>MT</Initials></Author><Author ValidYN="Y"><LastName>Christensen</LastName><ForeName>Bruce M</ForeName><Initials>BM</Initials></Author><Author ValidYN="Y"><LastName>Dimopoulos</LastName><ForeName>George</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI061576</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1 R01 AI061576-01A1</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 AI019769</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI19769</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI059492</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI019769</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 AI007414</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1 R01 AI059492-01A1</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>10</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Negl Trop Dis</MedlineTA><NlmUniqueID>101291488</NlmUniqueID><ISSNLinking>1935-2727</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Mol Microbiol. 2006 Jun;60(5):1194-204</RefSource><PMID 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UI="Q000635" MajorTopicYN="N">transmission</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005370" MajorTopicYN="N">Filarioidea</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005849" MajorTopicYN="N">Gerbillinae</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007303" MajorTopicYN="N">Insect Vectors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000469" MajorTopicYN="Y">parasitology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC2752998</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2009</Year><Month>04</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>09</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>10</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>12</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19823571</ArticleId><ArticleId IdType="doi">10.1371/journal.pntd.0000529</ArticleId><ArticleId IdType="pmc">PMC2752998</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Wisconsin</li></region></list><tree><noCountry><name sortKey="Aliota, Matthew T" sort="Aliota, Matthew T" uniqKey="Aliota M" first="Matthew T" last="Aliota">Matthew T. Aliota</name><name sortKey="Christensen, Bruce M" sort="Christensen, Bruce M" uniqKey="Christensen B" first="Bruce M" last="Christensen">Bruce M. Christensen</name><name sortKey="Dimopoulos, George" sort="Dimopoulos, George" uniqKey="Dimopoulos G" first="George" last="Dimopoulos">George Dimopoulos</name><name sortKey="Mayhew, George F" sort="Mayhew, George F" uniqKey="Mayhew G" first="George F" last="Mayhew">George F. Mayhew</name><name sortKey="Ramirez, Jose L" sort="Ramirez, Jose L" uniqKey="Ramirez J" first="Jose L" last="Ramirez">Jose L. Ramirez</name><name sortKey="Xi, Zhiyong" sort="Xi, Zhiyong" uniqKey="Xi Z" first="Zhiyong" last="Xi">Zhiyong Xi</name></noCountry><country name="États-Unis"><region name="Wisconsin"><name sortKey="Erickson, Sara M" sort="Erickson, Sara M" uniqKey="Erickson S" first="Sara M" last="Erickson">Sara M. Erickson</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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