Immunopathogenesis of dengue hemorrhagic fever: Contribution to the study of human liver lesions

Carregando...
Imagem de Miniatura
Citações na Scopus
42
Tipo de produção
article
Data de publicação
2014
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY-BLACKWELL
Autores
QUARESMA, Juarez Antonio Simoes
FERNANDES, Elaine Raniero
BRASIL, Roosecelis Araujo
BARROS, Vera
VASCONCELOS, Pedro Fernando C.
Citação
JOURNAL OF MEDICAL VIROLOGY, v.86, n.7, p.1193-1197, 2014
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Dengue infection is an important tropical disease worldwide. The host immune response has been studied in order to better understand lesion mechanisms. It was performed an immunohistochemical study in 14 specimens of liver from patients with dengue hemorrhagic fever (DHF) to characterize cytokines and some factors present in liver lesions and their possible role in the pathogenesis of hepatic injury. Portal tract and hepatic acinus presented high expression of TLR2, TLR3, IL6, and granzyme B. Hepatic acinus also presented iNOS, IL18, and TGF-beta. Cells expressing IL12, IL13, JAk1, STAT1, and NF-kappa B were rarely visualized. Treg cells foxp3+ were absent. TLR2 and TLR3 seem to participate in cellular activation and cytokine production. Cytotoxic response seems to play a role. Although TGF-beta promotes the activation of Foxp3+ regulatory T cells, IL6 can significantly suppresses their generation. The expression of Treg cells is diminished probably as a result of the high frequency of these cytokines. Both cytokines play a role in the increased vascular permeability and edema observed in dengue liver specimens, with consequent plasma leakage and severity of the disease. It was observed a regular expression of IL-18 in hepatocytes and lymphocytes of the inflammatory infiltrate in portal tract, which reflects the acute inflammatory response that occurs in the liver and contributes to hepatic injury. At least in part, the increased number of cells expressing IL-18 could play a role of ""up"" regulation of FasL and correlate to the phenomenon of apoptosis, a mechanism of destruction of hepatocytes in DHF. J. Med. Virol. 86:1193-1197, 2014. (c) 2013 Wiley Periodicals, Inc.
Palavras-chave
cytokines, immunopathology, liver, dengue hemorrhagic fever
Referências
  1. AKIRA S, 1993, ADV IMMUNOL, V54, P1, DOI 10.1016/S0065-2776(08)60532-5
  2. Belkaid Y, 2005, NAT IMMUNOL, V4, P841
  3. Bettelli E, 2006, NATURE, V441, P235, DOI 10.1038/nature04753
  4. BEYNON HLC, 1993, CLIN EXP IMMUNOL, V91, P314
  5. Bhakdi S, 1990, Southeast Asian J Trop Med Public Health, V21, P652
  6. BielefeldtOhmann H, 1997, TRENDS MICROBIOL, V5, P409, DOI 10.1016/S0966-842X(97)01126-8
  7. Brasil RA, 2005, THESIS U SAO PAULO
  8. Couvelard A, 1999, HUM PATHOL, V30, P1106, DOI 10.1016/S0046-8177(99)90230-7
  9. DING A, 1990, J IMMUNOL, V145, P940
  10. Gagnon SJ, 1999, J VIROL, V73, P3623
  11. HOBER D, 1993, AM J TROP MED HYG, V48, P324
  12. Hori S, 2003, SCIENCE, V299, P1057, DOI 10.1126/science.1079490
  13. HSUAN JJ, 1989, BRIT MED BULL, V45, P425
  14. Huerre MR, 2001, VIRCHOWS ARCH, V438, P107
  15. Hung NT, 2004, J INFECT DIS, V189, P221, DOI 10.1086/380762
  16. Kimura A, 2010, EUR J IMMUNOL, V40, P1830, DOI 10.1002/eji.201040391
  17. Kurane I, 2007, COMP IMMUNOL MICROB, V30, P329, DOI 10.1016/j.cimid.2007.05.010
  18. Lee YR, 2007, VIRUS RES, V126, P216, DOI 10.1016/j.virusres.2007.03.003
  19. Lin CF, 2005, J IMMUNOL, V174, P395
  20. Luhn K, 2007, J EXP MED, V204, P979, DOI 10.1084/jem.20061381
  21. Marianneau P, 1999, J VIROL, V73, P5201
  22. MARUO N, 1992, ENDOCRINOLOGY, V131, P710, DOI 10.1210/en.131.2.710
  23. Rothman AL, 1999, VIROLOGY, V257, P1, DOI 10.1006/viro.1999.9656
  24. Tsai YT, 2009, CELL MICROBIOL, V11, P604, DOI 10.1111/j.1462-5822.2008.01277.x