EPA protects against muscle damage in the mdx mouse model of Duchenne muscular dystrophy by promoting a shift from the M1 to M2 macrophage phenotype

Carvalho, Samara Camaçarí de; Apolinário, Letícia Montanholi; Matheus, Selma Maria Michelin; Neto, Humberto Santo; Marques, Maria Júlia

doi:10.1016/j.jneuroim.2013.09.007

Cited by 38 publications

(32 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recent studies indicated that EPA had beneficial effects on macrophage behavior in some disease models. A previous study conducted in the mdx mouse model regarding Duchenne muscular dystrophy indicated that in neuromuscular diseases, EPA decreased inflammation and necrosis in the dystrophic muscle by promoting a shift from the M1 to the M2 macrophage phenotype . In the present study we demonstrated that long‐term administration of EPA before and after MI promoted polarization, which is dominated by anti‐inflammatory M2 macrophages, and did not affect the total number of macrophages.…”

Section: Discussionsupporting

confidence: 66%

Long‐Term Administration of Eicosapentaenoic Acid Improves Post–Myocardial Infarction Cardiac Remodeling in Mice by Regulating Macrophage Polarization

Takamura

Kurokawa

Ootsuji

et al. 2017

JAHA

View full text Add to dashboard Cite

BackgroundConsumption of n‐3 fatty acids reduces the incidence of cardiovascular mortality in populations that consume diets rich in fish oil. Eicosapentaenoic acid (EPA) is an n‐3 fatty acid known to reduce the frequency of nonfatal coronary events; however, the frequency of mortality after myocardial infarction (MI) is not reduced. The aims of this study were to determine whether long‐term administration of EPA regulated cardiac remodeling after MI and to elucidate the underlying therapeutic mechanisms of EPA.Methods and ResultsC57BL/6J mice were divided into control (phosphate‐buffered saline–treated) and EPA‐treated groups. After 28 days of treatment, the mice were subjected to either sham surgery or MI by left anterior descending coronary artery ligation. Mortality due to MI or heart failure was significantly lower in the EPA‐treated mice than in the phosphate‐buffered saline–treated mice. However, the incidence of cardiac rupture was comparable between the EPA‐treated mice and the phosphate‐buffered saline–treated mice after MI. Echocardiographic tests indicated that EPA treatment attenuated post‐MI cardiac remodeling by preventing issues such as left ventricular systolic dysfunction and left ventricle dilatation 28 days after MI induction. Moreover, during the chronic remodeling phase, ie, 28 days after MI, flow cytometry demonstrated that EPA treatment significantly inhibited polarization toward proinflammatory M1 macrophages, but not anti‐inflammatory M2 macrophages, in the infarcted heart. Furthermore, EPA treatment attenuated fibrosis in the noninfarcted remote areas during the chronic phase.ConclusionsLong‐term administration of EPA improved the prognosis of and attenuated chronic cardiac remodeling after MI by modulating the activation of proinflammatory M1 macrophages.

show abstract

Section: Discussionsupporting

confidence: 66%

Long‐Term Administration of Eicosapentaenoic Acid Improves Post–Myocardial Infarction Cardiac Remodeling in Mice by Regulating Macrophage Polarization

Takamura

Kurokawa

Ootsuji

et al. 2017

JAHA

View full text Add to dashboard Cite

show abstract

“…Moreover, DHA inhibits IL-12 and IL-23 production and prevents the upregulation of MHC II and costimulatory molecules [38]. High consumption of n-3 PUFAs promotes a shift in macrophage polarization and protects the liver and muscle from pathological damage [39, 40]. Moreover, studies have shown that 2-week feeding of fish oil diet significantly decreases the numbers of CD8 + T cells in the lungs of influenza virus-infected mice, resulting in a high morbidity and mortality [41].…”

Section: Discussionmentioning

confidence: 99%

Chronic intake of high fish oil diet induces myeloid-derived suppressor cells to promote tumor growth

Sheng

Cheng

et al. 2014

Cancer Immunol Immunother

View full text Add to dashboard Cite

Omega-3 polyunsaturated fatty acids enriched fish oil exerts beneficial anti-inflammatory effects in animal models with acute and chronic inflammatory diseases. Myeloid-derived suppressor cells (MDSCs), comprised of myeloid progenitors and precursors of myeloid cells, play vital roles in cancer. How fish oil affects the generation of MDSCs and the tumor development remains largely unexplored. Here, we show that dietary intake of high fish oil diet suppresses CD8+ T cells activation and proliferation in vivo via elevated levels of MDSCs. Mechanistically, high fish oil diet induces the expression of immunosuppressive cytokine IL-10 and promotes myelopoiesis in the spleen as well as other peripheral tissues. The immature myeloid cells in the spleen exhibit morphological and functional characteristics of MDSCs with the capability to downregulate CD8+ T cells activation. Depletion of MDSCs using anti-Gr-1 antibody decreases the growth of subcutaneously transferred B16 melanoma in mice on high fish oil diet. Interestingly, diet-induced production of MDSCs is not solely dependent of the spleen, as splenectomy has no effect on the tumor progress. Our data show that the liver functions as an alternative extramedullary hematopoiesis organ to support MDSCs differentiation and maintain tumor growth. Taken together, our study provides a novel insight into the physiological effects of fish oil and points to MDSCs as a possible mediator linking dietary fish oil intake and immunosuppression in cancer immunosurveillance.

show abstract

“…Classical “pro-inflammatory” subpopulations of mononuclear phagocytes secrete more pro-inflammatory cytokines compared to non-classical alternatively-activated subpopulations [13]–[16], suggesting that intramuscular infiltration of classical subtypes may promote chronic muscle degeneration. Indeed, in the mdx mouse model of Duchenne muscular dystrophy, chronic muscle degeneration is in part caused by the classical pro-inflammatory Ly6C hi subset of circulating monocytes (MO) [17]. Human and rodent muscles undergoing fatty degeneration after RCT show dramatic co-localization of fat-rich regions with macrophages (MΦ) that contain intracellular lipid droplets [7], [8].…”

Section: Introductionmentioning

confidence: 99%

Quantitative Analysis of Immune Cell Subset Infiltration of Supraspinatus Muscle After Severe Rotator Cuff Injury

Krieger

Tellier

Ollukaren

et al. 2017

Regen. Eng. Transl. Med.

View full text Add to dashboard Cite

Rotator cuff tears cause muscle degeneration that is characterized by myofiber atrophy, fatty infiltration, and fibrosis and is minimally responsive to current treatment options. The underlying pathogenesis of rotator cuff muscle degeneration remains to be elucidated, and increasing evidence implicates immune cell infiltration as a significant factor. Because immune cells are comprised of highly heterogeneous subpopulations that exert divergent effects on injured tissue, understanding trafficking and accumulation of immune subpopulations may hold the key to more effective therapies. The present study quantifies subpopulations of immune cells infiltrating the murine supraspinatus muscle after severe rotator cuff injury that includes tenotomy and denervation. Rotator cuff injury stimulates dramatic infiltration of mononuclear phagocytes, enriches mononuclear phagocytes in non-classical subpopulations, and enriches T lymphocytes in TH and Treg subpopulations. The combination of tenotomy plus denervation significantly increases mononuclear phagocyte infiltration, enriches macrophages in the non-classical subpopulation, and decreases T lymphocyte enrichment in TH cells compared to tenotomy alone. Depletion of circulating monocytes via liposomal clodronate accelerates supraspinatus atrophy after tenotomy and denervation. The study may aid rational design of immunologically smart therapies that harness immune cells to enhance outcomes after rotator cuff tears.

show abstract

EPA protects against muscle damage in the mdx mouse model of Duchenne muscular dystrophy by promoting a shift from the M1 to M2 macrophage phenotype

Cited by 38 publications

References 39 publications

Long‐Term Administration of Eicosapentaenoic Acid Improves Post–Myocardial Infarction Cardiac Remodeling in Mice by Regulating Macrophage Polarization

Long‐Term Administration of Eicosapentaenoic Acid Improves Post–Myocardial Infarction Cardiac Remodeling in Mice by Regulating Macrophage Polarization

Chronic intake of high fish oil diet induces myeloid-derived suppressor cells to promote tumor growth

Quantitative Analysis of Immune Cell Subset Infiltration of Supraspinatus Muscle After Severe Rotator Cuff Injury

Contact Info

Product

Resources

About