Esophageal mucosa in HIV infection: A ""deeper"" look at this little spoken organ

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art_WERNECK-SILVA_Esophageal_mucosa_in_HIV_infection_A_deeper_look_2017.PDF (482.75 KB)
Citações na Scopus
1
Tipo de produção
article
Data de publicação
2017
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY
Autores
PATZINA, Roseli A.
Citação
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, v.32, n.11, p.1832-1838, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background and Aim: Although the esophagus is a common site of opportunistic infection in AIDS patients, little is known about the impact of HIV as well as opportunistic infection in the esophageal mucosa. Our aim is to analyze the esophageal immune profile in HIV+ patients with different immunological status with and without the opportunistic Candida infection. Methods: Immunohistochemistry to CD4+ and CD8+ T-cells, gamma-interferon, transforming growth factor-beta, interleukin (IL)-4, IL-6, IL-13, and IL-17 was performed in esophageal samples of 40 chronically HIV+ patients under highly active antiretroviral therapy (16 with Candida esophagitis, 12 virologically non-supressed with blood CD4 count < 500, and 12 virologically suppressed with blood CD4 count > 500; the latter two groups without esophageal candidiasis). The controls were 12 HIV-negative healthy individuals. Results: Esophageal CD4+ T-cell expression in HIV+ patients did not differ from the control group (P = 0.50). Mucosal CD8+ T-cell expression was significantly increased in HIV+ patients (P = 0.0018). Candida esophagitis and virologically non-supressed HIV+ patients with CD4 < 500 showed an increased expression of IL-17 and IL-6 with fewer expressions of gamma-interferon, more attenuated in the latter group. Transforming growth factor-beta was increased only in virologically suppressed HIV+ patients with CD4 > 500. IL-4 and IL-13 were similar to the control group. Conclusion: In contrast to CD8+ T-cell expression, esophageal CD4+ T-cell expression does not reflect the HIV+ patient's immunological status. T-helper 17 (Th17) response seems to play a role in the esophageal mucosa of virologically non-supressed HIV+ patients with blood CD4 < 500. Candida esophagitis showed a Th1/ Th17 response but seems to be dominantly regulated by the Th17 pathway.
Palavras-chave
candidiasis, esophagus, HIV, human, immunohistochemistry, mucosal immunity
URI
https://observatorio.fm.usp.br/handle/OPI/25675
Referências
  1. Bixler S. L., 2013, CLIN DEV IMMUNOL, V2013, DOI 10.1155/2013/852418
  2. Brenchley JM, 2013, MUCOSAL IMMUNOL, V6, P657, DOI 10.1038/mi.2013.15
  3. Carmack SW, 2009, ADV ANAT PATHOL, V16, P290, DOI 10.1097/PAP.0b013e3181b5073a
  4. Charton-Bain MC, 1999, HISTOPATHOLOGY, V34, P399
  5. Chun TW, 2008, J INFECT DIS, V197, P714, DOI 10.1086/527324
  6. Di Pilato V, 2016, ANN NY ACAD SCI, V1381, P21, DOI 10.1111/nyas.13127
  7. Dongari-Bagtzoglou A, 2005, J DENT RES, V84, P966, DOI 10.1177/154405910508401101
  8. Gaardbo JC, 2008, CLIN EXP IMMUNOL, V154, P80, DOI 10.1111/j.1365-2249.2008.03725.x
  9. Gladiator A, 2013, J IMMUNOL, V190, P521, DOI 10.4049/jimmunol.1202924
  10. Gordon SN, 2010, J IMMUNOL, V185, P5169, DOI 10.4049/jimmunol.1001801
  11. Guadalupe M, 2003, J VIROL, V77, P11708, DOI 10.1128/JVI.77.21.11708-11717.2003
  12. Hayes TL, 2013, AIDS, V27, P867, DOI 10.1097/QAD.0b013e32835d85b4
  13. Ivanov II, 2009, CELL, V139, P485, DOI 10.1016/j.cell.2009.09.033
  14. Jay L, 2007, J IMMUNOL, V198, P605
  15. Klatt NR, 2010, CURR OPIN HIV AIDS, V5, P135, DOI 10.1097/COH.0b013e3283364846
  16. Kolte L, 2009, CLIN EXP IMMUNOL, V155, P44, DOI 10.1111/j.1365-2249.2008.03803.x
  17. Kutteh WH, 2005, MUCOSAL IMMUNOLOGY, 3RD EDITION, P1631, DOI 10.1016/B978-012491543-5/50099-1
  18. Lim A, 2007, AIDS, V21, P1525, DOI 10.1097/QAD.0b013e32825eab8b
  19. Lind A, 2014, PLOS ONE, V9, DOI 10.1371/journal.pone.0106261
  20. Lucendo AJ, 2007, AM J SURG PATHOL, V31, P598, DOI 10.1097/01.pas.0000213392.49698.8c
  21. Macal M, 2008, MUCOSAL IMMUNOL, V1, P475, DOI 10.1038/mi.2008.35
  22. Macpherson AJ, 2013, SEMIN IMMUNOL, V25, P358, DOI 10.1016/j.smim.2013.09.004
  23. Martin J, 2012, PLOS ONE, V7
  24. Mattapallil JJ, 2005, NATURE, V434, P1093, DOI 10.1038/nature03501
  25. Mehandru S, 2004, J EXP MED, V200, P761, DOI 10.1084/jem.20041196
  26. Mehandru S, 2006, PLOS MED, V3, P2335, DOI 10.1371/journal.pmed.0040484
  27. Mowat AM, 1997, IMMUNOL REV, V156, P145, DOI 10.1111/j.1600-065X.1997.tb00966.x
  28. Nkuize M, 2010, HIV MED, V11, P412, DOI 10.1111/j.1468-1293.2009.00807.x
  29. Paiardini M, 2008, AIDS REV, V10, P36
  30. Resnick MB, 1999, HUM PATHOL, V30, P397, DOI 10.1016/S0046-8177(99)90114-4
  31. Rocha L, 2010, PATHOL RES PRACT, V206, P248, DOI 10.1016/j.prp.2009.12.004
  32. Rocha LP, 2011, AIDS RES HUM RETROV, V27, P511, DOI 10.1089/aid.2010.0184
  33. Spits H, 2013, NAT REV IMMUNOL, V13, P145, DOI 10.1038/nri3365
  34. Steele C, 2000, J INFECT DIS, V182, P1479, DOI 10.1086/315872
  35. Sutton CE, 2012, EUR J IMMUNOL, V42, P2221, DOI 10.1002/eji.201242569
  36. Takatori H, 2009, J EXP MED, V206, P35, DOI 10.1084/jem.20072713
  37. Tincati C, 2009, ANTIVIR THER, V14, P321
  38. Yue FY, 2008, J VIROL, V82, P6767, DOI 10.1128/JVI.02550-07
  39. Zuniga LA, 2013, IMMUNOL REV, V252, P78, DOI 10.1111/imr.12036

Coleções
Artigos e Materiais de Revistas Científicas - FM/MPT
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/06
Artigos e Materiais de Revistas Científicas - ODS/03