Hydrogen sulfide modulates chromatin remodeling and inflammatory mediator production in response to endotoxin, but does not play a role in the development of endotoxin tolerance

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art_RIOS_Hydrogen_sulfide_modulates_chromatin_remodeling_and_inflammatory_mediator_2016.PDF (2.02 MB)
Citações na Scopus
13
Tipo de produção
article
Data de publicação
2016
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
BIOMED CENTRAL LTD
Autores
OLAH, Gabor
GEROE, Domokos
SZCZESNY, Bartosz
SZABO, Csaba
Citação
JOURNAL OF INFLAMMATION-LONDON, v.13, article ID 10, 11p, 2016
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Pretreatment with low doses of LPS (lipopolysaccharide, bacterial endotoxin) reduces the pro-inflammatory response to a subsequent higher LPS dose, a phenomenon known as endotoxin tolerance. Moreover, hydrogen sulfide (H2S), an endogenous gaseous mediator (gasotransmitter) can exert anti-inflammatory effects. Here we investigated the potential role of H2S in the development of LPS tolerance. THP1 differentiated macrophages were pretreated with the H2S donor NaHS (1 mM) or the H2S biosynthesis inhibitor aminooxyacetic acid (AOAA, 1 mM). Methods: To induce tolerance, cells were treated with a low concentration of LPS (0.5 mu g/ml) for 4 or 24 h, and then treated with a high concentration of LPS (1 mu g/ml) for 4 h or 24 h. In in vivo studies, male wild-type and CSE-/- mice were randomized to the following groups: Control (vehicle); Endotoxemic saline for 3 days before the induction of endotoxemia with 10 mg/kg LPS) mg/kg; Tolerant (LPS at 1 mg/kg for 3 days, followed LPS at 10 mg/kg). Animals were sacrificed after 4 or 12 h; plasma IL-6 and TNF-alpha levels were measured. Changes in histone H3 and H4 acetylation were analyzed by Western blotting. Results: LPS tolerance decreased pro-inflammatory cytokine production. AOAA did not affect the effect of tolerance on reducing cytokine production. Treatment of the cells with the H2S donor reduced cytokine production. Induction of the tolerance increased the acetylation of H3; AOAA reduced histone acetylation. H2S donation increased histone acetylation. Tolerance did not affect the responses to H2S with respect to histone acetylation. Conclusions: In conclusion, both LPS tolerance and H2S donation decrease LPS-induced cytokine production in vitro and modulate histone acetylation. However, endogenous, CSE-derived H2S does not appear to play a significant role in the development of LPS tolerance.
Palavras-chave
Hydrogen sulfide, Endotoxin, Cytokines, Macrophages, Tolerance
URI
https://observatorio.fm.usp.br/handle/OPI/14134
Referências
  1. Yang G, 2006, FASEB J, V20, P553, DOI 10.1096/fj.05-4712fje
  2. West MA, 2002, CRIT CARE MED, V30, pS64, DOI 10.1097/00003246-200201001-00009
  3. Rios ECS, 2015, INT J MOL MED, V35, P1741, DOI 10.3892/ijmm.2015.2176
  4. Szabo C, 2007, NAT REV DRUG DISCOV, V6, P917, DOI 10.1038/nrd2425
  5. Szczesny B, 2014, NITRIC OXIDE-BIOL CH, V41, P120, DOI 10.1016/j.niox.2014.04.008
  6. Kimura Y, 2004, FASEB J, V18, P1165, DOI 10.1096/fj.04-1815fje
  7. Schaafsma W, 2015, BRAIN BEHAV IMMUN, V48, P205, DOI 10.1016/j.bbi.2015.03.013
  8. Yang GD, 2004, J BIOL CHEM, V279, P49199, DOI 10.1074/jbc.M408997200
  9. Pena OM, 2011, J IMMUNOL, V186, P7243, DOI 10.4049/jimmunol.1001952
  10. VINCENT JL, 1990, CRIT CARE MED, V18, pS70
  11. Foster SL, 2007, NATURE, V447, P972, DOI 10.1038/nature05836
  12. Suzuki K, 2011, P NATL ACAD SCI USA, V108, P13829, DOI 10.1073/pnas.1105121108
  13. Hinshaw LB, 1996, CRIT CARE MED, V24, P1072, DOI 10.1097/00003246-199606000-00031
  14. Wang R, 2012, PHYSIOL REV, V92, P791, DOI 10.1152/physrev.00017.2011
  15. El Gazzar M, 2009, MOL CELL BIOL, V29, P1959, DOI 10.1128/MCB.01862-08
  16. Woltmann A, 1998, LANGENBECK ARCH SURG, V383, P2, DOI 10.1007/s004230050085
  17. Fox B, 2012, J CELL MOL MED, V16, P896, DOI 10.1111/j.1582-4934.2011.01357.x
  18. Aslami H, 2013, CYTOKINE, V61, P614, DOI 10.1016/j.cyto.2012.11.018
  19. Li L, 2008, CIRCULATION, V117, P2351, DOI 10.1161/CIRCULATIONAHA.107.753467
  20. Fernandes ML, 2010, BRAZ J MED BIOL RES, V43, P860, DOI 10.1590/S0100-879X2010000900008
  21. Papapetropoulos A, 2015, BRIT J PHARMACOL, V172, P1633, DOI 10.1111/bph.12806
  22. Neagos J, 2015, AM J RESP CELL MOL, V53, P872, DOI 10.1165/rcmb.2015-0057OC
  23. Hirohashi N, 1996, INFECT IMMUN, V64, P1011
  24. Truong DH, 2006, DRUG METAB REV, V38, P733, DOI 10.1080/03602530600959607
  25. El Gazzar M, 2007, J BIOL CHEM, V282, P26857, DOI 10.1074/jbc.M704584200
  26. Ferlito M, 2014, J IMMUNOL, V192, P1806, DOI 10.4049/jimmunol.1300835
  27. Friedman G, 1998, CRIT CARE MED, V26, P2078, DOI 10.1097/00003246-199812000-00045
  28. Natoli G, 2006, FEBS LETT, V580, P2843, DOI 10.1016/j.febslet.2006.02.072
  29. Beutler B, 2003, NAT REV IMMUNOL, V3, P169, DOI 10.1038/nri1004
  30. Melo ES, 2010, BRAZ J MED BIOL RES, V43, P57, DOI 10.1590/S0100-879X2009007500027
  31. Asimakopoulou A, 2013, BRIT J PHARMACOL, V169, P922, DOI 10.1111/bph.12171
  32. Chan C, 2005, J IMMUNOL, V175, P461
  33. Angus DC, 2001, CRIT CARE MED, V29, P1303, DOI 10.1097/00003246-200107000-00002
  34. Yang GD, 2008, SCIENCE, V322, P587, DOI 10.1126/science.1162667
  35. Chen Hong Ping, 2015, Critical Reviews in Oncogenesis, V20, P35
  36. Xin H, 2016, ANTIOXID REDOX SIGN, V24, P70, DOI 10.1089/ars.2015.6315
  37. Liu TF, 2011, J BIOL CHEM, V286, P9856, DOI 10.1074/jbc.M110.196790
  38. McCuskey RS, 1996, CARDIOVASC RES, V32, P752, DOI 10.1016/S0008-6363(96)00113-7
  39. Coletta C, 2013, CURR VASC PHARMACOL, V11, P208
  40. McCall CE, 2007, AM J RESP CRIT CARE, V175, P763, DOI 10.1164/rccm.200610-1436CP
  41. Beurel E, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0025804
  42. Friedman Gilberto, 2008, Rev Bras Ter Intensiva, V20, P267, DOI 10.1590/S0103-507X2008000300010
  43. Seeley John J, 2013, Cold Spring Harb Symp Quant Biol, V78, P69, DOI 10.1101/sqb.2013.78.020040
  44. Szabo C, 2016, NAT REV DRUG DISCOV, V15, P185, DOI 10.1038/nrd.2015.1

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/51
Artigos e Materiais de Revistas Científicas - ODS/07