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Treatment in vitro with PPARα and PPARγ ligands drives M1-to-M2 polarization of macrophages from T. cruzi-infected mice.

Penas F, Mirkin GA, Vera M, Cevey Á, González CD, Gómez MI, Sales ME, Goren NB.

Biochim Biophys Acta. 2015 May;1852(5):893-904. doi: 10.1016/j.bbadis.2014.12.019. Epub 2014 Dec 31.


PPARγ ligand treatment inhibits cardiac inflammatory mediators induced by infection with different lethality strains of Trypanosoma cruzi.

Penas F, Mirkin GA, Hovsepian E, Cevey A, Caccuri R, Sales ME, Goren NB.

Biochim Biophys Acta. 2013 Jan;1832(1):239-48. doi: 10.1016/j.bbadis.2012.08.007. Epub 2012 Aug 16.


Modulation of inflammatory response and parasitism by 15-Deoxy-Δ(12,14) prostaglandin J(2) in Trypanosoma cruzi-infected cardiomyocytes.

Hovsepian E, Mirkin GA, Penas F, Manzano A, Bartrons R, Goren NB.

Int J Parasitol. 2011 Apr;41(5):553-62. doi: 10.1016/j.ijpara.2010.12.002. Epub 2011 Jan 6.


[Adipose-derived stem cells promote the polarization from M1 macrophages to M2 macrophages].

Yin X, Pang C, Bai L, Zhang Y, Geng L.

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2016 Mar;32(3):332-8. Chinese.


Timing of expression of inflammatory mediators in skeletal muscles from mice acutely infected with the RA strain of Trypanosoma cruzi.

Cutrullis RA, Postan M, Petray PB, Corral RS.

Pathobiology. 2009;76(4):170-80. doi: 10.1159/000218333. Epub 2009 Jun 29.


Hepatic injury associated with Trypanosoma cruzi infection is attenuated by treatment with 15-deoxy-Δ12,14 prostaglandin J2.

Penas FN, Cevey ÁC, Siffo S, Mirkin GA, Goren NB.

Exp Parasitol. 2016 Nov;170:100-108. doi: 10.1016/j.exppara.2016.09.015. Epub 2016 Sep 28.


Selective inhibition and augmentation of alternative macrophage activation by progesterone.

Menzies FM, Henriquez FL, Alexander J, Roberts CW.

Immunology. 2011 Nov;134(3):281-91. doi: 10.1111/j.1365-2567.2011.03488.x.


Peroxisome proliferator-activated receptor-γ-mediated polarization of macrophages in Neospora caninum infection.

He X, Gong P, Wei Z, Liu W, Wang W, Li J, Yang Z, Zhang X.

Exp Parasitol. 2017 Jul;178:37-44. doi: 10.1016/j.exppara.2017.05.002. Epub 2017 May 17.


Synergistic effect of peroxisome proliferator activated receptor-gamma and liver X receptor-alpha in the regulation of inflammation in macrophages.

Piraino G, Cook JA, O'Connor M, Hake PW, Burroughs TJ, Teti D, Zingarelli B.

Shock. 2006 Aug;26(2):146-53.


Programmed death ligand 2 regulates arginase induction and modifies Trypanosoma cruzi survival in macrophages during murine experimental infection.

Dulgerian LR, Garrido VV, Stempin CC, Cerbán FM.

Immunology. 2011 May;133(1):29-40. doi: 10.1111/j.1365-2567.2011.03406.x. Epub 2011 Feb 8.


Extracellular mycobacterial DnaK polarizes macrophages to the M2-like phenotype.

Lopes RL, Borges TJ, Araújo JF, Pinho NG, Bergamin LS, Battastini AM, Muraro SP, Souza AP, Zanin RF, Bonorino C.

PLoS One. 2014 Nov 24;9(11):e113441. doi: 10.1371/journal.pone.0113441. eCollection 2014.


Trypanosoma cruzi infection of cultured adipocytes results in an inflammatory phenotype.

Nagajyothi F, Desruisseaux MS, Thiruvur N, Weiss LM, Braunstein VL, Albanese C, Teixeira MM, de Almeida CJ, Lisanti MP, Scherer PE, Tanowitz HB.

Obesity (Silver Spring). 2008 Sep;16(9):1992-7.


MIF-driven activation of macrophages induces killing of intracellular Trypanosoma cruzi dependent on endogenous production of tumor necrosis factor, nitric oxide and reactive oxygen species.

Cutrullis RA, Petray PB, Corral RS.

Immunobiology. 2017 Feb;222(2):423-431. doi: 10.1016/j.imbio.2016.08.007. Epub 2016 Aug 28.


The adenosine-dependent angiogenic switch of macrophages to an M2-like phenotype is independent of interleukin-4 receptor alpha (IL-4Rα) signaling.

Ferrante CJ, Pinhal-Enfield G, Elson G, Cronstein BN, Hasko G, Outram S, Leibovich SJ.

Inflammation. 2013 Aug;36(4):921-31. doi: 10.1007/s10753-013-9621-3.


Inducible nitric oxide synthase and arginase expression in heart tissue during acute Trypanosoma cruzi infection in mice: arginase I is expressed in infiltrating CD68+ macrophages.

Cuervo H, Pineda MA, Aoki MP, Gea S, Fresno M, Gironès N.

J Infect Dis. 2008 Jun 15;197(12):1772-82. doi: 10.1086/529527.


Mannosyl-recognizing receptors induce an M1-like phenotype in macrophages of susceptible mice but an M2-like phenotype in mice resistant to a fungal infection.

Feriotti C, Loures FV, Frank de Araújo E, da Costa TA, Calich VL.

PLoS One. 2013;8(1):e54845. doi: 10.1371/journal.pone.0054845. Epub 2013 Jan 30.


PPARalpha agonists inhibit nitric oxide production by enhancing iNOS degradation in LPS-treated macrophages.

Paukkeri EL, Leppänen T, Sareila O, Vuolteenaho K, Kankaanranta H, Moilanen E.

Br J Pharmacol. 2007 Dec;152(7):1081-91. Epub 2007 Sep 24.


Azithromycin reduces exaggerated cytokine production by M1 alveolar macrophages in cystic fibrosis.

Meyer M, Huaux F, Gavilanes X, van den Brûle S, Lebecque P, Lo Re S, Lison D, Scholte B, Wallemacq P, Leal T.

Am J Respir Cell Mol Biol. 2009 Nov;41(5):590-602. doi: 10.1165/rcmb.2008-0155OC. Epub 2009 Feb 24.


Effects of macrophage-dependent peroxisome proliferator-activated receptor γ signalling on adhesion formation after abdominal surgery in an experimental model.

Hong GS, Schwandt T, Stein K, Schneiker B, Kummer MP, Heneka MT, Kitamura K, Kalff JC, Wehner S.

Br J Surg. 2015 Nov;102(12):1506-16. doi: 10.1002/bjs.9907. Epub 2015 Aug 27.


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