Peroxisome proliferator activated receptor γ is not necessary for the development of LPS-induced tolerance in macrophages

Immunology

Volumn 124, Issue 1, 2008, Pages 51-57

  Zingarelli, Basilia ^a,c   Fan, Hongkuan ^b   Ashton, Sarah ^b   Piraino, Giovanna ^c   Mangeshkar, Prajakta ^c   Cook, James A ^b  

^a CINCINNATI CHILDREN'S HOSPITAL MEDICAL CENTER   (United States)

^b MEDICAL UNIVERSITY OF SOUTH CAROLINA   (United States)

^c UNIVERSITY OF CINCINNATI COLLEGE OF MEDICINE   (United States)

Author keywords

Endotoxin; Inflammatory mediators; Macrophages; Transcription factors

Indexed keywords

2 CHLORO 5 NITROBENZANILIDE; BACTERIUM LIPOPOLYSACCHARIDE; NITRITE; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA; THROMBOXANE B2; TUMOR NECROSIS FACTOR ALPHA;

ANIMAL CELL; ANIMAL EXPERIMENT; ARTICLE; CONTROLLED STUDY; CYTOKINE RELEASE; EX VIVO STUDY; FUNCTIONAL PROTEOMICS; IMMUNOLOGICAL TOLERANCE; IMMUNOMODULATION; IN VITRO STUDY; INFLAMMATION; KNOCKOUT MOUSE; MALE; MOUSE; NONHUMAN; PERITONEUM MACROPHAGE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; RAT; WILD TYPE;

ANILIDES; ANIMALS; CELLS, CULTURED; DOSE-RESPONSE RELATIONSHIP, IMMUNOLOGIC; IMMUNE TOLERANCE; LIPOPOLYSACCHARIDES; MACROPHAGES, PERITONEAL; MALE; MICE; MICE, KNOCKOUT; PPAR GAMMA; RATS; RATS, LONG-EVANS; TUMOR NECROSIS FACTOR-ALPHA;

EID: 42149085179     PISSN: 00192805     EISSN: 13652567     Source Type: Journal    
DOI: 10.1111/j.1365-2567.2007.02734.x     Document Type: Article

References (23)

1. Rocchi S, Auwerx J. Peroxisome proliferator-activated receptor-γ: a versatile metabolic regulator. Ann Med 1999 31 : 342 51.
2. Jiang C, Ting AT, Seed B. PPARγ agonists inhibit production of monocyte inflammatory cytokines. Nature 1998 391 : 82 6.
3. Ricote M, Li AC, Willson TM, Kelly CJ, Glass CK. The peroxisome proliferator-activated receptor-γ is a negative regulator of macrophage activation. Nature 1998 391 : 79 82.
4. 2), a peroxisome proliferator-activated receptor-γ ligand, reduces tissue leukosequestration and mortality in endotoxic shock. Shock 2004 24 : 59 65.
5. 2 against the multiple organ failure caused by endotoxin. Crit Care Med 2004 32 : 826 31.
6. 2 and ciglitazone, reduces systemic inflammation in polymicrobial sepsis by modulation of signal transduction pathways. J Immunol 2003 171 : 6827 37.
7. 2 reduces the organ injury in hemorrhagic shock. Shock 2004 22 : 555 61.
8. Mathison JC, Virca GD, Wolfson E, Tobias PS, Glaser K, Ulevitch RJ. Adaptation to bacterial lipopolysaccharide controls lipopolysaccharide-induced tumor necrosis factor production in rabbit macrophages. J Clin Invest 1990 85 : 1108 18.
9. Rayhane N, Lortholary O, Fitting C, Callebert J, Huerre M, Dromer F, Cavaillon JM. Enhanced sensitivity of tumor necrosis factor/lymphotoxin-α- deficient mice to Cryptococcus neoformans infection despite increased levels of nitrite/nitrate, interferon-γ, and interleukin-12. J Infect Dis 1999 180 : 1637 47.
10. Astiz ME, Rackow EC, Still JG et al. Pretreatment of normal humans with monophosphoryl lipid A induces tolerance to endotoxin: a prospective, double-blind, randomized, controlled trial. Crit Care Med 1995 23 : 9 17.
11. Peck OM, Zingarelli B, Fan H, Teti G, Tempel G, Halushka PV, Cook JA. The phosphatidylinositol 3 kinase pathway regulates tolerance to lipopolysaccharide and priming responses to Staphylococcus aureus and lipopolysaccharide. Shock 2006 26 : 31 6.
12. Fan H, Cook JA. Molecular mechanisms of endotoxin tolerance. J Endotoxin Res 2004 10 : 71 84.
13. Cavaillon JM, Adrie C, Fitting C, Adib-Conquy M. Endotoxin tolerance: is there a clinical relevance? J Endotoxin Res 2003 9 : 101 7.
14. Leesnitzer LM, Parks DJ, Bledsoe RK. Functional consequences of cysteine modification in the ligand binding sites of peroxisome proliferator activated receptors by GW9662. Biochemistry 2002 41 : 6640 50.
15. Akiyama TE, Sakai S, Lambert G et al. Conditional disruption of the peroxisome proliferator-activated receptor gamma gene in mice results in lowered expression of ABCA1, ABCG1, and apoE in macrophages and reduced cholesterol efflux. Mol Cell Biol 2002 22 : 2607 19.
16. Zingarelli B, Hake PW, Cook JA. Inducible nitric oxide synthase is not required in the development of endotoxin tolerance in mice. Shock 2002 17 : 478 84.
17. Zingarelli B, Southan GJ, Gilad E, O'Connor M, Salzman AL, Szabo C. The inhibitory effects of mercaptoalkylguanidines on cyclo-oxygenase activity. Br J Pharmacol 1997 120 : 357 66.
18. Zingarelli B, Halushka PV, Caputi AP, Cook JA. Increased nitric oxide synthesis during the development of endotoxin tolerance. Shock 1995 3 : 102 8.
19. Zingarelli B, Chen H, Caputi AP, Halushka PV, Cook JA. Reorientation of macrophage mediator production in endotoxin tolerance. Prog Clin Biol Res 1995 392 : 529 37.
20. Fernando LP, Fernando AN, Ferlito M, Halushka PV, Cook JA. Suppression of Cox-2 and TNFα mRNA in endotoxin tolerance: effect of cycloheximide, antinomycin D, and okadaic acid. Shock 2000 14 : 128 33.
21. Collin M, Murch O, Thiemermann C. Peroxisome proliferator-activated receptor-γ antagonists GW9662 and T0070907 reduce the protective effects of lipopolysaccharide preconditioning against organ failure caused by endotoxemia. Crit Care Med 2006 34 : 1131 8.
22. Collin M, Abdelrahman M, Thiemermann C. Endogenous ligands of PPARγ reduce the liver injury in haemorrhagic shock. Eur J Pharmacol 2004 486 : 233 5.
23. Von Knethen AA, Brune B. Delayed activation of PPARγ by LPS and IFN-γ attenuates the oxidative burst in macrophages. FASEB J 2001 15 : 535 44.