Filaria-Induced Monocyte Dysfunction and Its Reversal following Treatment†
Identifieur interne : 001799 ( Pmc/Curation ); précédent : 001798; suivant : 001800Filaria-Induced Monocyte Dysfunction and Its Reversal following Treatment†
Auteurs : Roshanak Tolouei Semnani ; Paul B. Keiser ; Yaya I. Coulibaly ; Falaye Keita ; Abdallah A. Diallo ; Diakaridia Traore ; Dapa A. Diallo ; Ogobara K. Doumbo ; Sekou F. Traore ; Joseph Kubofcik ; Amy D. Klion ; Thomas B. NutmanSource :
- Infection and Immunity [ 0019-9567 ] ; 2006.
Abstract
Monocyte dysfunction in filarial infection has been proposed as one mechanism underlying the diminished antigen-specific T-cell response seen in patent lymphatic filariasis. Cytokine/chemokine production and gene expression in monocytes from filaria-infected patients and uninfected healthy donors were assessed unstimulated and in response to stimulation with
Url:
DOI: 10.1128/IAI.01106-05
PubMed: 16861626
PubMed Central: 1539612
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<front><div type="abstract" xml:lang="en"><p>Monocyte dysfunction in filarial infection has been proposed as one mechanism underlying the diminished antigen-specific T-cell response seen in patent lymphatic filariasis. Cytokine/chemokine production and gene expression in monocytes from filaria-infected patients and uninfected healthy donors were assessed unstimulated and in response to stimulation with <italic>Staphylococcus aureus</italic>
Cowan I bacteria plus gamma interferon both before and 8 months following treatment. Monocytes from filaria-infected individuals were studded with intracellular microfilarial antigens. Furthermore, monocytes from these individuals were less capable of producing interleukin-8 (IL-8), Exodus II, MIP-1α, MIP-1β, and IL-1α and preferentially expressed genes involved in apoptosis and adhesion compared with monocytes from uninfected donors. Eight months following treatment with a single dose of ivermectin-albendazole, some of these defects were reversed, with monocyte production of IL-8, IL-1α, MIP-1α, and IL-10 being comparable to that seen in the uninfected controls. In addition, a marked increase in mRNA expression of genes associated with protein metabolism, particularly heat shock proteins, was seen compared with pretreatment expression. These data suggest that the function and gene expression of monocytes in filaria-infected patients are altered but that this dysfunction is partially reversible following antifilarial treatment.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Infect Immun</journal-id>
<journal-id journal-id-type="publisher-id">iai</journal-id>
<journal-title>Infection and Immunity</journal-title>
<issn pub-type="ppub">0019-9567</issn>
<issn pub-type="epub">1098-5522</issn>
<publisher><publisher-name>American Society for Microbiology</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">16861626</article-id>
<article-id pub-id-type="pmc">1539612</article-id>
<article-id pub-id-type="publisher-id">1106-05</article-id>
<article-id pub-id-type="doi">10.1128/IAI.01106-05</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Cellular Microbiology: Pathogen-Host Cell Molecular Interactions</subject>
</subj-group>
</article-categories>
<title-group><article-title>Filaria-Induced Monocyte Dysfunction and Its Reversal following Treatment<xref ref-type="fn" rid="fn1">†</xref>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Semnani</surname>
<given-names>Roshanak Tolouei</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Keiser</surname>
<given-names>Paul B.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Coulibaly</surname>
<given-names>Yaya I.</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Keita</surname>
<given-names>Falaye</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Diallo</surname>
<given-names>Abdallah A.</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Traore</surname>
<given-names>Diakaridia</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Diallo</surname>
<given-names>Dapa A.</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Doumbo</surname>
<given-names>Ogobara K.</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Traore</surname>
<given-names>Sekou F.</given-names>
</name>
<xref ref-type="aff" rid="aff1">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kubofcik</surname>
<given-names>Joseph</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Klion</surname>
<given-names>Amy D.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nutman</surname>
<given-names>Thomas B.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
</contrib-group>
<aff id="aff1">Helminth Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland,<label>1</label>
Departments of Epidemiology and Parasitic Diseases, University of Mali School of Medicine, Pharmacy, and Dentistry, Bamako, Mali<label>2</label>
</aff>
<author-notes><fn id="cor1"><label>*</label>
<p>Corresponding author. Mailing address: LPD, NIAID, 4 Center Drive, Room 4/126, NIH, Bethesda, MD 20892. Phone: (301) 435-7873. Fax: (301) 480-3757. E-mail: <email>rsemnani@niaid.nih.gov</email>
.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><month>8</month>
<year>2006</year>
</pub-date>
<volume>74</volume>
<issue>8</issue>
<fpage>4409</fpage>
<lpage>4417</lpage>
<history><date date-type="received"><day>13</day>
<month>7</month>
<year>2005</year>
</date>
<date date-type="rev-recd"><day>30</day>
<month>8</month>
<year>2005</year>
</date>
<date date-type="accepted"><day>2</day>
<month>5</month>
<year>2006</year>
</date>
</history>
<copyright-statement>Copyright © 2006, American Society for Microbiology</copyright-statement>
<copyright-year>2006</copyright-year>
<self-uri xlink:title="pdf" xlink:href="zii00806004409.pdf"></self-uri>
<abstract><p>Monocyte dysfunction in filarial infection has been proposed as one mechanism underlying the diminished antigen-specific T-cell response seen in patent lymphatic filariasis. Cytokine/chemokine production and gene expression in monocytes from filaria-infected patients and uninfected healthy donors were assessed unstimulated and in response to stimulation with <italic>Staphylococcus aureus</italic>
Cowan I bacteria plus gamma interferon both before and 8 months following treatment. Monocytes from filaria-infected individuals were studded with intracellular microfilarial antigens. Furthermore, monocytes from these individuals were less capable of producing interleukin-8 (IL-8), Exodus II, MIP-1α, MIP-1β, and IL-1α and preferentially expressed genes involved in apoptosis and adhesion compared with monocytes from uninfected donors. Eight months following treatment with a single dose of ivermectin-albendazole, some of these defects were reversed, with monocyte production of IL-8, IL-1α, MIP-1α, and IL-10 being comparable to that seen in the uninfected controls. In addition, a marked increase in mRNA expression of genes associated with protein metabolism, particularly heat shock proteins, was seen compared with pretreatment expression. These data suggest that the function and gene expression of monocytes in filaria-infected patients are altered but that this dysfunction is partially reversible following antifilarial treatment.</p>
</abstract>
</article-meta>
<notes><fn-group><fn><p><italic>Editor:</italic>
J. F. Urban, Jr.</p>
</fn>
</fn-group>
</notes>
</front>
</pmc>
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