Hypertonic solution-induced preconditioning reduces inflammation and mortality rate

Imagem de Miniatura
Arquivos
art_PIMENTEL_Hypertonic_solutioninduced_preconditioning_reduces_inflammation_and_mortality_rate_2019.PDF (985.9 KB)
Citações na Scopus
1
Tipo de produção
article
Data de publicação
2019
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
BMC
Autores
ANDRADE, Mariana Macedo
Citação
JOURNAL OF INFLAMMATION-LONDON, v.16, article ID UNSP 16, 9p, 2019
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
BackgroundDysregulated inflammatory response is common cause of organ damage in critical care patients. Preconditioning/tolerance is a strategy to prevent exacerbated inflammation. The aim of this study is to analyze hypertonic saline 7.5% as a potential inducer of preconditioning that protect from a lethal dose of LPS and modulates systemic inflammatory profile in mice.MethodsMale Balb/C mice received intravenous (i.v.) injections of Hypertonic solution (NaCl 7.5%) (0.8ml) for 3days, on day 8th was challenged with LPS 15mg/kg. Controls with Saline 0.9%, urea and sorbitol were performed. Microarray of mRNA expression was analyzed from HS versus saline from macrophages to identified the pathways activated by HS.ResultsHS preconditioning reduced mortality after LPS injection as well reduced the cytokines release in plasma of the animals challenged by LPS. In order to check how HS induces a preconditioning state we measured plasma cytokines after each HS infusion. Repeated HS injections induced a state of preconditioning that reprograms the inflammatory response, resulting in reduced inflammatory cytokine production. A microarray of mRNA demonstrated that Hypertonic solution increased the expression of several genes in special Mapkbp1 and Atf3.Conclusionhypertonic solution induces preconditioning/tolerance reducing mortality and inflammatory response after LPS challenge.
Palavras-chave
Sepsis, Inflammation, Preconditioning, Hypertonic solution, Tolerance
URI
https://observatorio.fm.usp.br/handle/OPI/33027
Referências
  1. Almeida FM, 2016, J HEART LUNG TRANSPL, V35, P242, DOI 10.1016/j.healun.2015.06.012
  2. Angus DC, 2001, CRIT CARE MED, V29, P1303, DOI 10.1097/00003246-200107000-00002
  3. Botker HE, 2018, AM J PHYSIOL-HEART C, V314, pH1225, DOI 10.1152/ajpheart.00027.2018
  4. Cuschieri J, 2002, J IMMUNOL, V168, P1389, DOI 10.4049/jimmunol.168.3.1389
  5. Costa FLD, 2017, ACTA CIR BRAS, V32, P599, DOI 10.1590/s0102-865020170080000001
  6. DEFELIPPE J, 1980, LANCET, V2, P1002
  7. Fernandes CI, 2009, BRAZ J MED BIOL RES, V42, P892, DOI 10.1590/S0100-879X2009005000024
  8. Gao J, 2013, MOL CELL BIOL, V33, P3026, DOI 10.1128/MCB.00349-13
  9. Gedik N, 2017, SCI REP-UK, V7, DOI 10.1038/s41598-017-12833-2
  10. Gillis D, 2001, J MEMBRANE BIOL, V181, P205, DOI 10.1007/s00232-001-0023-3
  11. HuangFu WC, 2006, J BIOL CHEM, V281, P28802, DOI 10.1074/jbc.M603627200
  12. Kohns M, 2018, SHOCK
  13. Medzhitov R, 1998, CURR OPIN IMMUNOL, V10, P12, DOI 10.1016/S0952-7915(98)80024-1
  14. Melo ES, 2010, IMMUNOBIOLOGY, V215, P435, DOI 10.1016/j.imbio.2009.09.002
  15. Melo ES, 2010, MOL IMMUNOL, V47, P2587, DOI 10.1016/j.molimm.2010.06.011
  16. Niswander JM, 2007, BRAIN RES, V1186, P1, DOI 10.1016/j.brainres.2007.10.008
  17. Oreopoulos GD, 2004, HEPATOLOGY, V40, P211, DOI 10.1002/hep.20281
  18. Petroni RC, 2015, SHOCK, V44, P609, DOI 10.1097/SHK.0000000000000461
  19. Petroni RC, 2015, INFLAMMATION, V38, P2026, DOI 10.1007/s10753-015-0183-4
  20. Figueira ERR, 2010, SURGERY, V147, P415, DOI 10.1016/j.surg.2009.10.018
  21. Rhind SG, 2010, J NEUROINFLAMM, V7, DOI 10.1186/1742-2094-7-5
  22. Rizoli SB, 1999, J TRAUMA, V46, P794, DOI 10.1097/00005373-199905000-00006
  23. Schlesinger Thomas K., 1998, Frontiers in Bioscience, V3, pD1181
  24. SILVA MRF, 1987, AM J PHYSIOL, V253, pH751
  25. Singer M, 2016, INTENS CARE MED, V42, P2027, DOI 10.1007/s00134-016-4600-4
  26. Theobaldo MC, 2012, CLINICS, V67, P1463, DOI 10.6061/clinics/2012(12)18
  27. Thompson MR, 2009, J MOL MED, V87, P1053, DOI 10.1007/s00109-009-0520-x
  28. Uhlik MT, 2003, NAT CELL BIOL, V5, P1104, DOI 10.1038/ncb1071
  29. VELASCO IT, 1989, CRIT CARE MED, V17, P261, DOI 10.1097/00003246-198903000-00012
  30. VELASCO IT, 1980, AM J PHYSIOL, V239, pH664
  31. Wade CE, 2002, CRIT CARE, V6, P397
  32. Xie Y, 2018, CELL DEATH DIS, V9, DOI 10.1038/s41419-018-0358-7

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/02
Artigos e Materiais de Revistas Científicas - LIM/51