Rhesus macaque θ-defensin RTD-1 inhibits proinflammatory cytokine secretion and gene expression by inhibiting the activation of NF-κB and MAPK pathways
Identifieur interne : 000544 ( Ncbi/Merge ); précédent : 000543; suivant : 000545Rhesus macaque θ-defensin RTD-1 inhibits proinflammatory cytokine secretion and gene expression by inhibiting the activation of NF-κB and MAPK pathways
Auteurs : Prasad Tongaonkar ; Katie K. Trinh ; Justin B. Schaal ; Dat Tran ; Percio S. Gulko ; André J. Ouellette ; Michael E. SelstedSource :
- Journal of Leukocyte Biology [ 0741-5400 ] ; 2015.
Abstract
The anti-inflammatory effects of θ-defensin RTD-1 are mediated by cell signaling pathways that down-regulate expression of pro-inflammatory cytokines.
Url:
DOI: 10.1189/jlb.3A0315-102R
PubMed: 26269197
PubMed Central: 4661038
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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Leukoc Biol</journal-id><journal-id journal-id-type="iso-abbrev">J. Leukoc. Biol</journal-id><journal-id journal-id-type="hwp">jleub</journal-id><journal-id journal-id-type="pmc">jleub</journal-id><journal-id journal-id-type="publisher-id">JLB</journal-id><journal-title-group><journal-title>Journal of Leukocyte Biology</journal-title></journal-title-group><issn pub-type="ppub">0741-5400</issn><issn pub-type="epub">1938-3673</issn><publisher><publisher-name>Society for Leukocyte Biology</publisher-name><publisher-loc>Bethesda, MD, USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26269197</article-id><article-id pub-id-type="pmc">4661038</article-id><article-id pub-id-type="publisher-id">JLB_3A0315-102R</article-id><article-id pub-id-type="doi">10.1189/jlb.3A0315-102R</article-id><article-categories><subj-group subj-group-type="heading"><subject>Inflammation, Extracellular Mediators, & Effector Molecules</subject></subj-group></article-categories><title-group><article-title>Rhesus macaque θ-defensin RTD-1 inhibits proinflammatory cytokine secretion and gene expression by inhibiting the activation of NF-κB and MAPK pathways</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Tongaonkar</surname><given-names>Prasad</given-names></name><xref ref-type="aff" rid="aff1">*</xref><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Trinh</surname><given-names>Katie K.</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Schaal</surname><given-names>Justin B.</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Tran</surname><given-names>Dat</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Gulko</surname><given-names>Percio S.</given-names></name><xref ref-type="aff" rid="aff2"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ouellette</surname><given-names>André J.</given-names></name><xref ref-type="aff" rid="aff1">*</xref></contrib><contrib contrib-type="author"><name><surname>Selsted</surname><given-names>Michael E.</given-names></name><xref ref-type="aff" rid="aff1">*</xref><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><aff><target id="aff1" target-type="aff">*</target>Department of Pathology and Laboratory Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California, USA; and<target id="aff2" target-type="aff"><sup>†</sup></target>Division of Rheumatology, Department of Medicine, The Icahn School of Medicine at Mount Sinai, New York, New York, USA</aff></contrib-group><author-notes><corresp id="cor1"><label>1</label>Correspondence: Department of Pathology and Laboratory Medicine, Keck School of Medicine, University of Southern California, Los Angeles, 7504 NRT, 1450 Biggy St., Los Angeles, CA 90033, USA. E-mail: <email>tongaonk@usc.edu</email> (P.T.) and <email>selsted@med.usc.edu</email> (M.E.S.)</corresp></author-notes><pub-date pub-type="ppub"><month>12</month><year>2015</year></pub-date><pub-date pub-type="epub"><day>12</day><month>8</month><year>2015</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>12</month><year>2016</year></pub-date><pmc-comment> PMC Release delay is 12 months and
0 days and was based on the
<volume>98</volume><issue>6</issue><fpage>1061</fpage><lpage>1070</lpage><history><date date-type="received"><day>10</day><month>3</month><year>2015</year></date><date date-type="rev-recd"><day>18</day><month>6</month><year>2015</year></date><date date-type="accepted"><day>12</day><month>7</month><year>2015</year></date></history><permissions><copyright-statement>© Society for Leukocyte Biology</copyright-statement><copyright-year>2015</copyright-year><copyright-holder>Society for Leukocyte Biology</copyright-holder></permissions><self-uri xlink:title="pdf" xlink:href="jleub3A0315-102R.pdf"></self-uri><abstract abstract-type="precis"><p>The anti-inflammatory effects of θ-defensin RTD-1 are mediated by cell signaling pathways that down-regulate expression of pro-inflammatory cytokines.</p></abstract><abstract><p>θ-Defensins are pleiotropic, macrocyclic peptides that are expressed uniquely in Old World monkeys. The peptides are potent, broad-spectrum microbicides that also modulate inflammatory responses in vitro and in animal models of viral infection and polymicrobial sepsis. θ-Defensins suppress proinflammatory cytokine secretion by leukocytes stimulated with diverse Toll-like receptor (TLR) ligands. Studies were performed to delineate anti-inflammatory mechanisms of rhesus θ-defensin 1 (RTD-1), the most abundant θ-defensin isoform in macaque granulocytes. RTD-1 reduced the secretion of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-8 in lipopolysaccharide (LPS)-stimulated human blood monocytes and THP-1 macrophages, and this was accompanied by inhibition of nuclear factor κB (NF-κB) activation and mitogen-activated protein kinase (MAPK) pathways. Peptide inhibition of NF-κB activation occurred following stimulation of extracellular (TLRs 1/2 and 4) and intracellular (TLR9) receptors. Although RTD-1 did not inhibit MAPK in unstimulated cells, it induced phosphorylation of Akt in otherwise untreated monocytes and THP-1 cells. In the latter, this occurred within 10 min of RTD-1 treatment and produced a sustained elevation of phosphorylated Akt (pAkt) for at least 4 h. pAkt is a negative regulator of MAPK and NF-κB activation. RTD-1 inhibited IκBα degradation and p38 MAPK phosphorylation, and stimulated Akt phosphorylation in LPS-treated human primary monocytes and THP-1 macrophages. Specific inhibition of phosphatidylinositol 3-kinase (PI3K) blocked RTD-1-stimulated Akt phosphorylation and reversed the suppression of NF-κB activation by the peptide. These studies indicate that the anti-inflammatory properties of θ-defensins are mediated by activation of the PI3K/Akt pathway and suppression of proinflammatory signals in immune-stimulated cells.</p></abstract><kwd-group><kwd>TLR</kwd><kwd>Akt</kwd><kwd>IκBα</kwd><kwd>THP-1</kwd><kwd>monocytes</kwd></kwd-group><counts><page-count count="10"></page-count></counts><custom-meta-group><custom-meta><meta-name> DJS Export </meta-name><meta-value>v1</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Gulko, Percio S" sort="Gulko, Percio S" uniqKey="Gulko P" first="Percio S." last="Gulko">Percio S. Gulko</name><name sortKey="Ouellette, Andre J" sort="Ouellette, Andre J" uniqKey="Ouellette A" first="André J." last="Ouellette">André J. Ouellette</name><name sortKey="Schaal, Justin B" sort="Schaal, Justin B" uniqKey="Schaal J" first="Justin B." last="Schaal">Justin B. Schaal</name><name sortKey="Selsted, Michael E" sort="Selsted, Michael E" uniqKey="Selsted M" first="Michael E." last="Selsted">Michael E. Selsted</name><name sortKey="Tongaonkar, Prasad" sort="Tongaonkar, Prasad" uniqKey="Tongaonkar P" first="Prasad" last="Tongaonkar">Prasad Tongaonkar</name><name sortKey="Tran, Dat" sort="Tran, Dat" uniqKey="Tran D" first="Dat" last="Tran">Dat Tran</name><name sortKey="Trinh, Katie K" sort="Trinh, Katie K" uniqKey="Trinh K" first="Katie K." last="Trinh">Katie K. Trinh</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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