Leishmania donovani Lipophosphoglycan Increases Macrophage-Dependent Chemotaxis of CXCR6-Expressing Cells via CXCL16 Induction.
Identifieur interne : 000303 ( Main/Exploration ); précédent : 000302; suivant : 000304Leishmania donovani Lipophosphoglycan Increases Macrophage-Dependent Chemotaxis of CXCR6-Expressing Cells via CXCL16 Induction.
Auteurs : Visnu Chaparro [Canada] ; Louis-Philippe Leroux [Canada] ; Aude Zimmermann [Canada] ; Armando Jardim [Canada] ; Brent Johnston [Canada] ; Albert Descoteaux [Canada] ; Maritza Jaramillo [Canada]Source :
- Infection and immunity [ 1098-5522 ] ; 2019.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Chimiokine CXCL16 (immunologie), Chimiotaxie (immunologie), Glycosphingolipides (immunologie), Humains (MeSH), Interactions hôte-parasite (immunologie), Leishmania donovani (immunologie), Leishmaniose viscérale (immunologie), Modèles animaux de maladie humaine (MeSH), Souris (MeSH), Souris de lignée BALB C (MeSH), Souris de lignée C57BL (MeSH).
- MESH :
English descriptors
- KwdEn :
- Animals (MeSH), Chemokine CXCL16 (immunology), Chemotaxis (immunology), Disease Models, Animal (MeSH), Glycosphingolipids (immunology), Host-Parasite Interactions (immunology), Humans (MeSH), Leishmania donovani (immunology), Leishmaniasis, Visceral (immunology), Mice (MeSH), Mice, Inbred BALB C (MeSH), Mice, Inbred C57BL (MeSH).
- MESH :
- chemical , immunology : Chemokine CXCL16, Glycosphingolipids.
- immunology : Chemotaxis, Host-Parasite Interactions, Leishmania donovani, Leishmaniasis, Visceral.
- Animals, Disease Models, Animal, Humans, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL.
Abstract
CXCL16 is a multifunctional chemokine that is highly expressed by macrophages and other immune cells in response to bacterial and viral pathogens; however, little is known regarding the role of CXCL16 during parasitic infections. The protozoan parasite Leishmania donovani is the causative agent of visceral leishmaniasis. Even though chemokine production is a host defense mechanism during infection, subversion of the host chemokine system constitutes a survival strategy adopted by the parasite. Here, we report that L. donovani promastigotes upregulate CXCL16 synthesis and secretion by bone marrow-derived macrophages (BMDM). In contrast to wild-type parasites, a strain deficient in the virulence factor lipophosphoglycan (LPG) failed to induce CXCL16 production. Consistent with this, cell treatment with purified L. donovani LPG augmented CXCL16 expression and secretion. Notably, the ability of BMDM to promote migration of cells expressing CXCR6, the cognate receptor of CXCL16, was augmented upon L. donovani infection in a CXCL16- and LPG-dependent manner. Mechanistically, CXCL16 induction by L. donovani required the activity of AKT and the mechanistic target of rapamycin (mTOR) but was independent of Toll-like receptor signaling. Collectively, these data provide evidence that CXCL16 is part of the inflammatory response elicited by L. donovani LPG in vitro Further investigation using CXCL16 knockout mice is required to determine whether this chemokine contributes to the pathogenesis of visceral leishmaniasis and to elucidate the underlying molecular mechanisms.
DOI: 10.1128/IAI.00064-19
PubMed: 30804103
PubMed Central: PMC6479025
Affiliations:
Links toward previous steps (curation, corpus...)
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last="Chaparro">Visnu Chaparro</name><affiliation wicri:level="1"><nlm:affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Leroux, Louis Philippe" sort="Leroux, Louis Philippe" uniqKey="Leroux L" first="Louis-Philippe" last="Leroux">Louis-Philippe Leroux</name><affiliation wicri:level="1"><nlm:affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Zimmermann, Aude" sort="Zimmermann, Aude" uniqKey="Zimmermann A" first="Aude" last="Zimmermann">Aude Zimmermann</name><affiliation wicri:level="1"><nlm:affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Jardim, Armando" sort="Jardim, Armando" uniqKey="Jardim A" first="Armando" last="Jardim">Armando Jardim</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Parasitology, McGill University, Sainte-Anne-de-Bellevue, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Institute of Parasitology, McGill University, Sainte-Anne-de-Bellevue, Quebec</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Johnston, Brent" sort="Johnston, Brent" uniqKey="Johnston B" first="Brent" last="Johnston">Brent Johnston</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Microbiology and Immunology and Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Departments of Microbiology and Immunology and Pediatrics, Dalhousie University, Halifax, Nova Scotia</wicri:regionArea><wicri:noRegion>Nova Scotia</wicri:noRegion></affiliation></author><author><name sortKey="Descoteaux, Albert" sort="Descoteaux, Albert" uniqKey="Descoteaux A" first="Albert" last="Descoteaux">Albert Descoteaux</name><affiliation wicri:level="1"><nlm:affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Jaramillo, Maritza" sort="Jaramillo, Maritza" uniqKey="Jaramillo M" first="Maritza" last="Jaramillo">Maritza Jaramillo</name><affiliation wicri:level="1"><nlm:affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada maritza.jaramillo@iaf.inrs.ca.</nlm:affiliation><country wicri:rule="url">Canada</country><wicri:regionArea>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author></analytic><series><title level="j">Infection and immunity</title><idno type="eISSN">1098-5522</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Chemokine CXCL16 (immunology)</term><term>Chemotaxis (immunology)</term><term>Disease Models, Animal (MeSH)</term><term>Glycosphingolipids (immunology)</term><term>Host-Parasite Interactions (immunology)</term><term>Humans (MeSH)</term><term>Leishmania donovani (immunology)</term><term>Leishmaniasis, Visceral (immunology)</term><term>Mice (MeSH)</term><term>Mice, Inbred BALB C (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Chimiokine CXCL16 (immunologie)</term><term>Chimiotaxie (immunologie)</term><term>Glycosphingolipides (immunologie)</term><term>Humains (MeSH)</term><term>Interactions hôte-parasite (immunologie)</term><term>Leishmania donovani (immunologie)</term><term>Leishmaniose viscérale (immunologie)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Souris (MeSH)</term><term>Souris de lignée BALB C (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Chemokine CXCL16</term><term>Glycosphingolipids</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Chimiokine CXCL16</term><term>Chimiotaxie</term><term>Glycosphingolipides</term><term>Interactions hôte-parasite</term><term>Leishmania donovani</term><term>Leishmaniose viscérale</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Chemotaxis</term><term>Host-Parasite Interactions</term><term>Leishmania donovani</term><term>Leishmaniasis, Visceral</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">CXCL16 is a multifunctional chemokine that is highly expressed by macrophages and other immune cells in response to bacterial and viral pathogens; however, little is known regarding the role of CXCL16 during parasitic infections. The protozoan parasite <i>Leishmania donovani</i> is the causative agent of visceral leishmaniasis. Even though chemokine production is a host defense mechanism during infection, subversion of the host chemokine system constitutes a survival strategy adopted by the parasite. Here, we report that <i>L. donovani</i> promastigotes upregulate CXCL16 synthesis and secretion by bone marrow-derived macrophages (BMDM). In contrast to wild-type parasites, a strain deficient in the virulence factor lipophosphoglycan (LPG) failed to induce CXCL16 production. Consistent with this, cell treatment with purified <i>L. donovani</i> LPG augmented CXCL16 expression and secretion. Notably, the ability of BMDM to promote migration of cells expressing CXCR6, the cognate receptor of CXCL16, was augmented upon <i>L. donovani</i> infection in a CXCL16- and LPG-dependent manner. Mechanistically, CXCL16 induction by <i>L. donovani</i> required the activity of AKT and the mechanistic target of rapamycin (mTOR) but was independent of Toll-like receptor signaling. Collectively, these data provide evidence that CXCL16 is part of the inflammatory response elicited by <i>L. donovani</i> LPG <i>in vitro</i> Further investigation using CXCL16 knockout mice is required to determine whether this chemokine contributes to the pathogenesis of visceral leishmaniasis and to elucidate the underlying molecular mechanisms.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30804103</PMID><DateCompleted><Year>2019</Year><Month>09</Month><Day>16</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>09</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1098-5522</ISSN><JournalIssue CitedMedium="Internet"><Volume>87</Volume><Issue>5</Issue><PubDate><Year>2019</Year><Month>03</Month></PubDate></JournalIssue><Title>Infection and immunity</Title><ISOAbbreviation>Infect Immun</ISOAbbreviation></Journal><ArticleTitle>Leishmania donovani Lipophosphoglycan Increases Macrophage-Dependent Chemotaxis of CXCR6-Expressing Cells via CXCL16 Induction.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">e00064-19</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1128/IAI.00064-19</ELocationID><Abstract><AbstractText>CXCL16 is a multifunctional chemokine that is highly expressed by macrophages and other immune cells in response to bacterial and viral pathogens; however, little is known regarding the role of CXCL16 during parasitic infections. The protozoan parasite <i>Leishmania donovani</i> is the causative agent of visceral leishmaniasis. Even though chemokine production is a host defense mechanism during infection, subversion of the host chemokine system constitutes a survival strategy adopted by the parasite. Here, we report that <i>L. donovani</i> promastigotes upregulate CXCL16 synthesis and secretion by bone marrow-derived macrophages (BMDM). In contrast to wild-type parasites, a strain deficient in the virulence factor lipophosphoglycan (LPG) failed to induce CXCL16 production. Consistent with this, cell treatment with purified <i>L. donovani</i> LPG augmented CXCL16 expression and secretion. Notably, the ability of BMDM to promote migration of cells expressing CXCR6, the cognate receptor of CXCL16, was augmented upon <i>L. donovani</i> infection in a CXCL16- and LPG-dependent manner. Mechanistically, CXCL16 induction by <i>L. donovani</i> required the activity of AKT and the mechanistic target of rapamycin (mTOR) but was independent of Toll-like receptor signaling. Collectively, these data provide evidence that CXCL16 is part of the inflammatory response elicited by <i>L. donovani</i> LPG <i>in vitro</i> Further investigation using CXCL16 knockout mice is required to determine whether this chemokine contributes to the pathogenesis of visceral leishmaniasis and to elucidate the underlying molecular mechanisms.</AbstractText><CopyrightInformation>Copyright © 2019 American Society for Microbiology.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chaparro</LastName><ForeName>Visnu</ForeName><Initials>V</Initials><Identifier Source="ORCID">0000-0001-6880-9234</Identifier><AffiliationInfo><Affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leroux</LastName><ForeName>Louis-Philippe</ForeName><Initials>LP</Initials><Identifier Source="ORCID">0000-0002-9736-1827</Identifier><AffiliationInfo><Affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zimmermann</LastName><ForeName>Aude</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jardim</LastName><ForeName>Armando</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute of Parasitology, McGill University, Sainte-Anne-de-Bellevue, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Johnston</LastName><ForeName>Brent</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Departments of Microbiology and Immunology and Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Descoteaux</LastName><ForeName>Albert</ForeName><Initials>A</Initials><Identifier Source="ORCID">0000-0002-0633-5309</Identifier><AffiliationInfo><Affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jaramillo</LastName><ForeName>Maritza</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-1910-5684</Identifier><AffiliationInfo><Affiliation>Institut National de la Recherche Scientifique-Institut Armand-Frappier, Laval, Quebec, Canada maritza.jaramillo@iaf.inrs.ca.</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></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>04</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Infect Immun</MedlineTA><NlmUniqueID>0246127</NlmUniqueID><ISSNLinking>0019-9567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000075743">Chemokine CXCL16</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006028">Glycosphingolipids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C008290">lipophosphonoglycan</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000075743" MajorTopicYN="N">Chemokine CXCL16</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002633" MajorTopicYN="N">Chemotaxis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006028" MajorTopicYN="N">Glycosphingolipids</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006790" MajorTopicYN="N">Host-Parasite Interactions</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007893" MajorTopicYN="N">Leishmania donovani</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007898" MajorTopicYN="N">Leishmaniasis, Visceral</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">CXCL16</Keyword><Keyword MajorTopicYN="Y">Leishmania
</Keyword><Keyword MajorTopicYN="Y">cell signaling</Keyword><Keyword MajorTopicYN="Y">chemokine</Keyword><Keyword MajorTopicYN="Y">inflammation</Keyword><Keyword MajorTopicYN="Y">lipophosphoglycan</Keyword><Keyword MajorTopicYN="Y">macrophage</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>01</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>02</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>2</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>9</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>2</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId 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