The Severity of Cecal Ligature and Puncture-Induced Sepsis Correlates with the Degree of Encephalopathy, but the Sepsis Does Not Lead to Acute Activation of Spleen Lymphocytes in Mice

Imagem de Miniatura
Arquivos
art_JEREMIAS_The_Severity_of_Cecal_Ligature_and_PunctureInduced_Sepsis_2016.PDF (1.06 MB)
Citações na Scopus
10
Tipo de produção
article
Data de publicação
2016
Editora
HUMANA PRESS INC
DOI
Indexadores
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Autores
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
MOLECULAR NEUROBIOLOGY, v.53, n.5, p.3389-3399, 2016
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Septic encephalopathy represents the most frequently observed form of encephalopathy in intensive care units. Interactions between the immune and nervous systems have been observed in experimental sepsis. Therefore, the aim of the current study was to characterize the effect of different severities of sepsis on encephalopathy and the inflammatory profile of the spleen. We hypothesized that different grades of sepsis severity would lead to variations in encephalopathy and activation of spleen cells. We induced sepsis of different severities in Balb/c mice by cecal ligature and puncture (CLP). Six and 12 h after CLP induction, behavioral impairment was assessed by the SmithKline/Harwell/Imperial College/Royal Hospital/Phenotype Assessment (SHIRPA) test. The animals were then killed, and the plasma, spleen, and hippocampus were removed. Levels of the encephalopathy marker S100 beta were measured in plasma. Spleens were weighed and then a characterization of splenic lymphocytes was performed by flow cytometry (cytotoxic T lymphocyte, T helper lymphocytes, B lymphocytes, T regulatory cells, and Th17 cells). Cytokine levels in the spleen and hippocampus were determined by enzyme-linked immunosorbent assay (ELISA), and cytokine levels in plasma were performed with MilliPlexA (R) technology. Our results showed that behavioral impairment as measured by the SHIRPA test and elevation in plasma S100 beta levels were significant in moderate and severe CLP groups compared to those in the sham control group. Regarding immunological alterations, we were unable to observe changes in the weights of the spleen and the profile of lymphocytes 6 h after CLP. However, several cytokines, including IL-6, IL-10, and IL-1 beta, were increased in spleen and plasma. In conclusion, we observed variations in encephalopathy as measured by plasma S100 beta, which were mediated by the severity of sepsis; however, we did not observe a different activation of spleen cells 6 h post-CLP, despite evidence of inflammation. Taken together, our data indicate that the severity of sepsis impacts the brain in absence of a change in the spleen lymphocyte profile.
Palavras-chave
Sepsis, Inflammation, SHIRPA, Septic encephalopathy, Lymphocytes
URI
https://observatorio.fm.usp.br/handle/OPI/16086
Referências
  1. Andreazza AC, 2007, J PSYCHIATR RES, V41, P523, DOI 10.1016/j.jpsychires.2006.07.013
  2. Barbeiro DF, 2011, IMMUNOBIOLOGY, V216, P302, DOI 10.1016/j.imbio.2010.08.002
  3. Barichello T, 2005, CRIT CARE MED, V33, P221, DOI 10.1097/01.CCM.0000150741.12906.BD
  4. Biberthaler P, 2006, SHOCK, V25, P446, DOI 10.1097/01.shk.0000209534.61058.35
  5. Biberthaler P, 2001, WORLD J SURG, V25, P93
  6. Blackwell TS, 1996, BRIT J ANAESTH, V77, P110
  7. Blyth BJ, 2009, J NEUROTRAUM, V26, P1497, DOI 10.1089/neu.2008-0738
  8. Borovikova LV, 2000, NATURE, V405, P458
  9. Bown MJ, 2001, EUR J VASC ENDOVASC, V22, P485, DOI 10.1053/ejvs.2001.1522
  10. Brooks HF, 2007, METAB BRAIN DIS, V22, P353, DOI 10.1007/s11011-007-9058-1
  11. CASEY LC, 1993, ANN INTERN MED, V119, P771
  12. Castoldi A, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0037584
  13. Comim CM, 2011, J NEURAL TRANSM, V118, P213, DOI 10.1007/s00702-010-0502-8
  14. Comim CM, 2011, INTENS CARE MED, V37, P711, DOI 10.1007/s00134-011-2151-2
  15. Damas P, 1997, CRIT CARE MED, V25, P405, DOI 10.1097/00003246-199703000-00006
  16. Da Silva FP, 2007, SEPSE
  17. [Anonymous], 2001, INT J BIOCHEM CELL B, DOI 10.1016/S1357-2725(01)00046-2
  18. Ebersoldt M, 2007, INTENS CARE MED, V33, P941, DOI 10.1007/s00134-007-0622-2
  19. Gomez HG, 2014, CRIT CARE MED, V42, P771, DOI 10.1097/CCM.0000000000000100
  20. Griffin EW, 2013, J NEUROSCI, V33, P15248, DOI 10.1523/JNEUROSCI.6361-11.2013
  21. GRIFFIN WST, 1989, P NATL ACAD SCI USA, V86, P7611
  22. Hiraki S, 2012, SURGERY, V151, P313, DOI 10.1016/j.surg.2011.07.019
  23. Hoesel LM, 2006, IMMUNOL RES, V34, P133, DOI 10.1385/IR:34:2:133
  24. Hotchkiss RS, 2003, NEW ENGL J MED, V348, P138, DOI 10.1056/NEJMra021333
  25. Hu YM, 2014, SHOCK, V4, P115
  26. Huston JM, 2006, J EXP MED, V203, P1623, DOI 10.1084/jem.20052362
  27. Imamura Y, 2011, NEUROSCIENCE, V187, P63, DOI 10.1016/j.neuroscience.2011.04.063
  28. Ingebrigtsen T, 1999, NEUROSURGERY, V45, P468, DOI 10.1097/00006123-199909000-00010
  29. Lackner P, 2006, NEUROPATH APPL NEURO, V32, P177, DOI 10.1111/j.1365-2990.2006.00706.x
  30. Lorigados CB, 2011, ENDOCR METAB IMMUNE, V10, P274
  31. Melo ES, 2011, MOL IMMUNOL, V47, P2587
  32. Melo ES, 2001, IMMUNOBIOLOGY, V215, P435
  33. Missler U, 1997, STROKE, V28, P1956
  34. Netto CBO, 2006, CLIN CHIM ACTA, V364, P275, DOI 10.1016/j.cca.2005.07.028
  35. Ono S, 2013, SURGERY, V153, P262, DOI 10.1016/j.surg.2012.06.023
  36. Osler W, 1908, BRIT MED J, V1908, P1470
  37. Pavlov VA, 2007, CRIT CARE MED, V35, P1139, DOI 10.1097/01.CCM.0000259381.56526.96
  38. Peskind ER, 2001, NEUROCHEM INT, V39, P409, DOI 10.1016/S0197-0186(01)00048-1
  39. Pozo AL, 2009, BLOOD REV, V23, P105, DOI 10.1016/j.blre.2008.10.001
  40. Pytel P, 2009, CURR OPIN NEUROL, V22, P283, DOI 10.1097/WCO.0b013e32832b3101
  41. Ringer TM, 2011, OPEN CRIT CARE MED J, V4, P2
  42. Ritter C, 2004, LANCET, V364, P498, DOI 10.1016/S0140-6736(04)16799-8
  43. Rogers DC, 1997, MAMM GENOME, V8, P711, DOI 10.1007/s003359900551
  44. Rosas-Ballina M, 2008, P NATL ACAD SCI USA, V105, P11008, DOI 10.1073/pnas.0803237105
  45. Rothermundt M, 2004, INT REV NEUROBIOL, V59, P445
  46. Ruan S, 2009, J NEUROTRAUM, V26, P1655, DOI 10.1089/neu.2009-0928
  47. Semmler A, 2005, J CHEM NEUROANAT, V30, P144, DOI 10.1016/j.jchemneu.2005.07.003
  48. Shimizu I, 1999, BRAIN RES, V830, P94, DOI 10.1016/S0006-8993(99)01396-7
  49. Szatmari S, 2010, CRIT CARE, V14, DOI 10.1186/cc8939
  50. Texereau J, 2004, CRIT CARE MED, V32, pS313, DOI 10.1097/01.CMM.0000126363.46191.DC
  51. Tracey KJ, 2002, NATURE, V420, P853, DOI 10.1038/nature01321
  52. Valdes-Ferrer SI, 2013, J INTERN MED, V274, P381, DOI 10.1111/joim.12104
  53. van Westerloo DJ, 2005, J INFECT DIS, V191, P2138, DOI 10.1086/430323
  54. Vanden Berghe T, 2014, AM J RESP CRIT CARE, V189, P282, DOI 10.1164/rccm.201308-1535OC
  55. Vandijck DM, 2006, ACTA CLIN BELG, V61, P220
  56. Wheeler AP, 1999, NEW ENGL J MED, V340, P207, DOI 10.1056/NEJM199901213400307
  57. Zenaide Paula Veriato, 2013, Rev. bras. ter. intensiva, V25, P56, DOI 10.1590/S0103-507X2013000100011
  58. Ziaja M, 2012, FOLIA NEUROPATHOL, V50, P231, DOI 10.5114/fn.2012.30523

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