ArticleBioMed research international2013
PPAR activation induces M1 macrophage polarization via cPLA₂-COX-2 inhibition, activating ROS production against Leishmania mexicana.
Article in BioMed research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Lipid Mediators in Host-Pathogen Interactions duringACS infectious diseases · 2026Review
- Oxidative Stress and Survival ofExpert reviews in molecular medicine · 2025Review
- The Functions of Cytokines in the Cardiac Immunopathogenesis of Chagas Disease.Pathogens (Basel, Switzerland) · 2024Review
- Mitochondrial oxidative damage reprograms lipid metabolism of renal tubular epithelial cells in the diabetic kidney.Cellular and molecular life sciences : CMLS · 2024Article
- Analysis of clinical cure outcome, macrophages number, cytokines levels and expression of annexin-A1 in the cutaneous infection in patients with Leishmania braziliensis.Revista da Sociedade Brasileira de Medicina Tropical · 2024Article
- Medium-chain fatty acids modify macrophage expression of metabolic and inflammatory genes in a PPAR β/δ-dependent manner.Scientific reports · 2023Article
- The roles of COX-2 in protozoan infection.Frontiers in immunology · 2023Review
- Article
- Hepatic macrophage mediated immune response in liver steatosis driven carcinogenesis.Frontiers in oncology · 2022Review
- In vitro and in vivo study of the pathogenic role of PPARα in experimental periodontitis.Journal of applied oral science : revista FOB · 2022Article
- IFN-γ and PPARδ influence the efficacy and retention of multipotent adult progenitor cells in graft vs host disease.Stem cells translational medicine · 2021Article
- Macrophage Polarization in the Skin Lesion Caused by Neotropical Species ofJournal of immunology research · 2021Article
- Transcription Factors Interplay Orchestrates the Immune-Metabolic Response ofFrontiers in cellular and infection microbiology · 2021Review
- Unbalanced production of LTBEmerging microbes & infections · 2020Article
- Detection of amastigotes and histopathological alterations in the thymus of Leishmania infantum-infected dogs.Immunity, inflammation and disease · 2020Article
- Macrophage Polarization in Leishmaniasis: Broadening Horizons.Frontiers in immunology · 2018Review
- Integrative Approaches to Understand the Mastery in Manipulation of Host Cytokine Networks by Protozoan Parasites with Emphasis onFrontiers in immunology · 2018Review
- Leishmania infantum lipophosphoglycan induced-Prostaglandin EScientific reports · 2017Article
- Moderate-intensity exercise alters markers of alternative activation in circulating monocytes in females: a putative role for PPARγ.European journal of applied physiology · 2016Article
- An M1-like Macrophage Polarization in Decidual Tissue during Spontaneous Preterm Labor That Is Attenuated by Rosiglitazone Treatment.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Defence against Leishmania depends upon Th1 inflammatory response and, a major problem in susceptible models, is the turnoff of the leishmanicidal activity of macrophages with IL-10, IL-4, and COX-2 upregulation, as well as immunosuppressive PGE2, all together inhibiting the respiratory burst. Peroxisome proliferator-activated receptors (PPAR) activation is responsible for macrophages polarization on Leishmania susceptible models where microbicide functions are deactivated. In this paper, we demonstrated that, at least for L. mexicana, PPAR activation, mainly PPAR γ , induced macrophage activation through their polarization towards M1 profile with the increase of microbicide activity against intracellular pathogen L. mexicana. PPAR activation induced IL-10 downregulation, whereas the production of proinflammatory cytokines such as TNF- α , IL-1 β , and IL-6 remained high. Moreover, PPAR agonists treatment induced the deactivation of cPLA2-COX-2-prostaglandins pathway together with an increase in TLR4 expression, all of whose criteria meet the M1 macrophage profile. Finally, parasite burden, in treated macrophages, was lower than that in infected nontreated macrophages, most probably associated with the increase of respiratory burst in these treated cells. Based on the above data, we conclude that PPAR agonists used in this work induces M1 macrophages polarization via inhibition of cPLA2 and the increase of aggressive microbicidal activity via reactive oxygen species (ROS) production.
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