The TLR4-Active Morphine Metabolite Morphine-3-Glucuronide Does Not Elicit Macrophage Classical Activation In Vitro
Identifieur interne : 003F69 ( Ncbi/Checkpoint ); précédent : 003F68; suivant : 003F70The TLR4-Active Morphine Metabolite Morphine-3-Glucuronide Does Not Elicit Macrophage Classical Activation In Vitro
Auteurs : Samira Khabbazi [Australie] ; Nan Xie [Australie] ; Wenjun Pu [Australie] ; Yannick Goumon [France] ; Marie-Odile Parat [Australie]Source :
- Frontiers in Pharmacology [ 1663-9812 ] ; 2016.
Abstract
Macrophages are abundant in the tumor microenvironment where they adopt a pro-tumor phenotype following alternative polarization induced by paracrine factors from cancer and stromal cells. In contrast, classically activated macrophages have tumoricidal activities, such that the polarization of tumor-associated macrophages has become a novel therapeutic target. Toll-like receptor 4 engagement promotes classical activation of macrophages, and recent literature suggests TLR4 agonism to prevent metastasis and promote survival in experimental metastasis models. A growing number of studies indicate that TLR4 can respond to opioids, including the opioid receptor-inactive morphine metabolite morphine-3-glucuronide (M3G). We measured the activation of TLR4 in a reporter cell line exogenously expressing TLR4 and TLR4 co-receptors, and confirmed that M3G weakly but significantly activates TLR4. We hypothesized that M3G would promote the expression of classical activation signature genes in macrophages
Url:
DOI: 10.3389/fphar.2016.00441
PubMed: 27909407
PubMed Central: 5112272
Affiliations:
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The TLR4-Active Morphine Metabolite Morphine-3-Glucuronide Does Not Elicit Macrophage Classical Activation <italic>In Vitro</italic>
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<front><div type="abstract" xml:lang="en"><p>Macrophages are abundant in the tumor microenvironment where they adopt a pro-tumor phenotype following alternative polarization induced by paracrine factors from cancer and stromal cells. In contrast, classically activated macrophages have tumoricidal activities, such that the polarization of tumor-associated macrophages has become a novel therapeutic target. Toll-like receptor 4 engagement promotes classical activation of macrophages, and recent literature suggests TLR4 agonism to prevent metastasis and promote survival in experimental metastasis models. A growing number of studies indicate that TLR4 can respond to opioids, including the opioid receptor-inactive morphine metabolite morphine-3-glucuronide (M3G). We measured the activation of TLR4 in a reporter cell line exogenously expressing TLR4 and TLR4 co-receptors, and confirmed that M3G weakly but significantly activates TLR4. We hypothesized that M3G would promote the expression of classical activation signature genes in macrophages <italic>in vitro</italic>
. We exposed mouse and human macrophage cell lines to M3G or the TLR4 activator lipopolysaccharide (LPS), alone or in combination with interferon gamma (IFN-γ). The classical macrophage activation markers tested were iNOS, CD86, IL-6, or TNF-α in RAW 264.7 cells and IL-6, IL-12, IL-23, TNF-α, CXCL10, and CXCL11 in THP1 cells. Our results show that despite exhibiting TLR4-activation ability, M3G does not elicit the expression of classical activation markers in LPS-responsive macrophages.</p>
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</TEI>
<affiliations><list><country><li>Australie</li>
<li>France</li>
</country>
</list>
<tree><country name="Australie"><noRegion><name sortKey="Khabbazi, Samira" sort="Khabbazi, Samira" uniqKey="Khabbazi S" first="Samira" last="Khabbazi">Samira Khabbazi</name>
</noRegion>
<name sortKey="Parat, Marie Odile" sort="Parat, Marie Odile" uniqKey="Parat M" first="Marie-Odile" last="Parat">Marie-Odile Parat</name>
<name sortKey="Pu, Wenjun" sort="Pu, Wenjun" uniqKey="Pu W" first="Wenjun" last="Pu">Wenjun Pu</name>
<name sortKey="Xie, Nan" sort="Xie, Nan" uniqKey="Xie N" first="Nan" last="Xie">Nan Xie</name>
</country>
<country name="France"><noRegion><name sortKey="Goumon, Yannick" sort="Goumon, Yannick" uniqKey="Goumon Y" first="Yannick" last="Goumon">Yannick Goumon</name>
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</record>
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