Foxp3 Expression and Nitric Oxide Production in Peripheral Blood Mononuclear Cells of Communicants with Pulmonary Tuberculosis

Carregando...
Imagem de Miniatura
Citações na Scopus
0
Tipo de produção
article
Data de publicação
2013
Editora
WILEY-BLACKWELL
Indexadores
Título da Revista
ISSN da Revista
Título do Volume
Autores
CAVALCANTI, Y. V. N.
ALMEIDA, T. M. de
ALMEIDA, A. F. de
LUCENA-SILVA, N.
PEREIRA, V. R. A.
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, v.78, n.1, p.79-84, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
The understanding of the mechanisms involved in the immune response is of significant relevance to the control of tuberculosis (TB), especially in individuals living with patients with TB. To characterize the nitric oxide (NO) production and the Foxp3 marker expression in this population, peripheral blood mononuclear cells of intradomiciliary contacts of individuals with pulmonary tuberculosis with (CTb, susceptible) and without (STb, resistant) previous history of active infection were stimulated in vitro with Mycobacterium tuberculosis antigen (TbAg) and with the mitogen Concanavalin A for 24 and 48h. The groups analysed did not present significant difference in the Foxp3 mRNA expression nor in the NO production. Negative correlation (P=0.09) between NO and Foxp3 after a 48-h stimulation with TbAg was observed in the STb group. In this group, after a 24-h culture stimulated with TbAg (P=0.03), this same correlation was observed. In comparison with the cytokines previously studied by our group (Cavalcanti etal., 2009), a positive correlation was observed between IL-10 and Foxp3 after a 48-h culture of cells from communicants susceptible to tuberculosis (STb) stimulated with TbAg (P=0.04). Evaluating the entire population, a positive correlation was observed between the cytokine TNF- and the Foxp3 marker in the cultures stimulated for 24 (P=0.03) and 48 (P=0.02) hours with TbAg. Therefore, considering the similarity in the exposure and the individual capacity of responding to the contact with M. tuberculosis, the present study contributes to the comprehension of the immune regulation in individuals living with patients with TB.
Palavras-chave
Referências
  1. Belkaid Y, 2007, NAT REV IMMUNOL, V7, P875, DOI 10.1038/nri2189
  2. Campbell DJ, 2007, NAT REV IMMUNOL, V7, P305, DOI 10.1038/nr2061
  3. Carvalho ACC, 2002, PULMAO, V11, P95
  4. Cavalcanti YVN, 2009, J CLIN LAB ANAL, V23, P57, DOI 10.1002/jcla.20290
  5. Chegou Novel N, 2009, BMC Pulm Med, V9, P21, DOI 10.1186/1471-2466-9-21
  6. Chegou NN, 2012, BMC INFECT DIS, V12, DOI 10.1186/1471-2334-12-10
  7. Churina EG, 2012, TUBERC RES TREAT, V2012, P1
  8. Danvider PSD, 2011, PLOSONE, V6
  9. Fiuza de Melo FA, 1995, B PNEUMOLOGIA SANITA, V1, P56
  10. FLYNN JL, 1993, J EXP MED, V178, P2249, DOI 10.1084/jem.178.6.2249
  11. Gupta A, 2012, IMMUNOBIOLOGY, V217, P363, DOI 10.1016/j.imbio.2011.07.008
  12. Guyot-Revol V, 2006, AM J RESP CRIT CARE, V173, P803, DOI 10.1164/rccm.200508-1294OC
  13. Harari A, 2011, NAT MED, V17, P372, DOI 10.1038/nm.2299
  14. Hesseling AC, 2009, THORAX, V64, P840, DOI 10.1136/thx.2007.085340
  15. HIBBS JB, 1988, BIOCHEM BIOPH RES CO, V157, P87, DOI 10.1016/S0006-291X(88)80015-9
  16. Hougardy JM, 2007, AM J RESP CRIT CARE, V176, P409, DOI 10.1164/rccm.200701-084OC
  17. Jonna I, 2012, PLOS ONE, V7
  18. Khader SA, 2007, NAT IMMUNOL, V8, P369, DOI 10.1038/ni1449
  19. Kinjo Y, 2002, J IMMUNOL, V169, P323
  20. LAEMMLI UK, 1970, NATURE, V227, P680, DOI 10.1038/227680a0
  21. Lee SW, 2011, J IMMUNOL, V186, P6972, DOI 10.4049/jimmunol.1100485
  22. Lin PL, 2010, J IMMUNOL, V185, P15, DOI 10.4049/jimmunol.0903856
  23. Lin YG, 1996, INFECT IMMUN, V64, P1351
  24. Lucena-Silva N, 2010, J EPIDEMIOL COMMUN H, V64, P513, DOI 10.1136/jech.2008.086801
  25. Martin IV, 2011, FRONT MICROBIOL, V2, P105
  26. Melo KM, 2009, REV BRAS ALER IMUNOP, V32, P184
  27. Ministerio da Saude, 2010, PROGR NAC CONTR TUB
  28. Ministerio da Saude, 2002, CAD AT BAS
  29. Mohan VP, 2001, INFECT IMMUN, V69, P1847, DOI 10.1128/IAI.69.3.1847-1855.2001
  30. Nicholson S, 1996, J EXP MED, V183, P2293, DOI 10.1084/jem.183.5.2293
  31. Niedbala W, 2007, P NATL ACAD SCI USA, V104, P15478, DOI 10.1073/pnas.0703725104
  32. Pereira MG, 1999, EPIDEMIOLOGIA TEORIA
  33. Rahman S, 2009, AM J PATHOL, V174, P2211, DOI 10.2353/ajpath.2009.080941
  34. Raja A, 2004, INDIAN J MED RES, V120, P213
  35. READ SM, 1981, ANAL BIOCHEM, V116, P53, DOI 10.1016/0003-2697(81)90321-3
  36. Ribeiro-Rodrigues R, 2006, CLIN EXP IMMUNOL, V144, P25, DOI 10.1111/j.1365-2249.2006.03027.x
  37. Sharma PK, 2009, AM J RESP CRIT CARE, V179, P1061, DOI 10.1164/rccm.200804-529OC
  38. Tomioka H, 2011, J INFECT CHEMOTHER, V17, P302, DOI 10.1007/s10156-010-0177-y
  39. World Health Organization, 2011, GLOB TUB CONTR
  40. Wu YQ, 2006, CELL, V126, P375, DOI 10.1016/j.cell.2006.05.042
  41. ZHANG M, 1995, INFECT IMMUN, V63, P3231
  42. Zuniga J, 2012, CLIN DEV IMMUNOL, V2012, P1