open access

Vol 77, No 5 (2009)
ORIGINAL PAPERS
Published online: 2009-08-12
Submitted: 2013-02-22
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Comparison of Th1 and Th2 response in the blood of tuberculous patients and healthy contacts

Jolanta Winek, Urszula Demkow, Ewa Rowińska-Zakrzewska, Małgorzata Szołkowska, Małgorzata Filewska, Jacek Jagodziński, Kazimierz Roszkowski-Śliż
Pneumonol Alergol Pol 2009;77(5):446-452.

open access

Vol 77, No 5 (2009)
ORIGINAL PAPERS
Published online: 2009-08-12
Submitted: 2013-02-22

Abstract


Introduction: Th1 response is known to play a dominant role in the resistance to tuberculosis. Nevertheless, IFN gamma levels are frequently increased in tuberculous patients, especially at the site of the disease. It is also possible that the shift toward Th2 response is responsible for the loss of resistance. The aim of this study was to compare the Th1 function of peripheral blood cells and the levels of antimycobacterial antibodies in the serum of culture positive tuberculosis patients and healthy tuberculosis (Tb) contacts. The correlation between the levels of antimycobacterial antibodies and Th1 function of blood cells was also evaluated.
Material and methods: The material consisted of 51 tuberculous patients and 20 healthy persons, close contacts of tuberculosis patients. The ability of peripheral blood cells to secrete IFN gamma and IL-2 was estimated in whole blood cultures with PHA, PWM and tuberculin. The levels of IFN gamma and IL-2 in the supernatants of cultures was estimated via a commercial ELISA test. The levels of antimycobacterial antibodies was measured with commercial immunoenzymatic kits detecting IgG antibodies against 38 kDa+16 kDa and IgG, IgA and IgM antibodies to 38 kDa + lipoarabinomannan (LAM).
Results: No difference was found in the secretion of IFN gamma and IL-2 after stimulation with PHA and PWM between the patients and contacts. The secretion of IFN gamma after stimulation with tuberculin was even greater in tuberculous patients than in contacts. The levels of IgG and IgA (38 kDa+LAM) were higher in tuberculous patients than in contacts. There was a negative correlation between the level of IgG anti 38 kDa+LAM and the ability of peripheral blood cells to secrete IFN gamma after non-specific stimulation in patients with tuberculosis.
Conclusions: Our study confirms the hypothesis that it is not the diminished production of Th1 cytokines, but rather the parallel overproduction of Th2 cytokines, which are essential in the development of tuberculosis.

Abstract


Introduction: Th1 response is known to play a dominant role in the resistance to tuberculosis. Nevertheless, IFN gamma levels are frequently increased in tuberculous patients, especially at the site of the disease. It is also possible that the shift toward Th2 response is responsible for the loss of resistance. The aim of this study was to compare the Th1 function of peripheral blood cells and the levels of antimycobacterial antibodies in the serum of culture positive tuberculosis patients and healthy tuberculosis (Tb) contacts. The correlation between the levels of antimycobacterial antibodies and Th1 function of blood cells was also evaluated.
Material and methods: The material consisted of 51 tuberculous patients and 20 healthy persons, close contacts of tuberculosis patients. The ability of peripheral blood cells to secrete IFN gamma and IL-2 was estimated in whole blood cultures with PHA, PWM and tuberculin. The levels of IFN gamma and IL-2 in the supernatants of cultures was estimated via a commercial ELISA test. The levels of antimycobacterial antibodies was measured with commercial immunoenzymatic kits detecting IgG antibodies against 38 kDa+16 kDa and IgG, IgA and IgM antibodies to 38 kDa + lipoarabinomannan (LAM).
Results: No difference was found in the secretion of IFN gamma and IL-2 after stimulation with PHA and PWM between the patients and contacts. The secretion of IFN gamma after stimulation with tuberculin was even greater in tuberculous patients than in contacts. The levels of IgG and IgA (38 kDa+LAM) were higher in tuberculous patients than in contacts. There was a negative correlation between the level of IgG anti 38 kDa+LAM and the ability of peripheral blood cells to secrete IFN gamma after non-specific stimulation in patients with tuberculosis.
Conclusions: Our study confirms the hypothesis that it is not the diminished production of Th1 cytokines, but rather the parallel overproduction of Th2 cytokines, which are essential in the development of tuberculosis.
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Keywords

Th-1; Th2 response in tuberculosis; IFN gamma; IL-2; antimycobacterial antibodies

About this article
Title

Comparison of Th1 and Th2 response in the blood of tuberculous patients and healthy contacts

Journal

Advances in Respiratory Medicine

Issue

Vol 77, No 5 (2009)

Pages

446-452

Published online

2009-08-12

Bibliographic record

Pneumonol Alergol Pol 2009;77(5):446-452.

Keywords

Th-1
Th2 response in tuberculosis
IFN gamma
IL-2
antimycobacterial antibodies

Authors

Jolanta Winek
Urszula Demkow
Ewa Rowińska-Zakrzewska
Małgorzata Szołkowska
Małgorzata Filewska
Jacek Jagodziński
Kazimierz Roszkowski-Śliż

References (22)
  1. Newport MJ, Nejentsev S. Genetics of susceptibility to tuberculosis in humans. Monaldi Arch Chest Dis. 2004; 61(2): 102–111.
  2. Morosini M, Meloni F, et al. Marone Bianco A. The assessment of IFN-g and its regulatory cytokines in the plasma and bronchoalveolar lavage fluid of patients with active pulmonary tuberculosis. Int. J. Tuberc. Lung Dis. 2003; 7: 994–1000.
  3. García M, Vargas JA, Castejón R, et al. Flow-cytometric assessment of lymphocyte cytokine production in tuberculosis. Tuberculosis (Edinb). 2002; 82(1): 37–41.
  4. Jo EK, Park JK, Dockrell HM. Dynamics of cytokine generation in patients with active pulmonary tuberculosis. Curr Opin Infect Dis. 2003; 16(3): 205–210.
  5. Demissie A, Abebe M, Aseffa A, et al. Healthy Individuals That Control a Latent Infection with Mycobacterium tuberculosis Express High Levels of Th1 Cytokines and the IL-4 Antagonist IL-4 2. The Journal of Immunology. 2004; 172(11): 6938–6943.
  6. Dheda K, Chang JS, Breen R, et al. In VivoandIn VitroStudies of a Novel Cytokine, Interleukin 4δ2, in Pulmonary Tuberculosis. American Journal of Respiratory and Critical Care Medicine. 2005; 172(4): 501–508.
  7. Dheda K, Chang JS, Huggett JF, et al. The stability of mRNA encoding IL-4 is increased in pulmonary tuberculosis, while stability of mRNA encoding the antagonistic splice variant, IL-4delta2, is not. Tuberculosis (Edinb). 2007; 87(3): 237–241.
  8. Elsässer-Beile U, von Kleist S, Gallati H. Evaluation of a test system for measuring cytokine production in human whole blood cell cultures. J Immunol Methods. 1991; 139(2): 191–195.
  9. Elliott AM, Hurst TJ, Balyeku MN, et al. The immune response to Mycobacterium tuberculosis in HIV-infected and uninfected adults in Uganda: application of a whole blood cytokine assay in an epidemiological study. Int J Tuberc Lung Dis. 1999; 3(3): 239–247.
  10. Morosini M, Meloni F, Uccelli M, et al. Ex vivo evaluation of PPD-specific IFN-gamma or IL-5 secreting cells in the peripheral blood and lungs of patients with tuberculosis. Int J Tuberc Lung Dis. 2005; 9(7): 753–759.
  11. de Castro Cunha RM, Kallas EG, Rodrigues DS, et al. Interferon-gamma and tumour necrosis factor-alpha production by CD4+ T and CD8+ T lymphocytes in AIDS patients with tuberculosis. Clin Exp Immunol. 2005; 140(3): 491–497.
  12. Toossi Z, Kleinhenz ME, Ellner JJ. Defective interleukin 2 production and responsiveness in human pulmonary tuberculosis. J Exp Med. 1986; 163(5): 1162–1172.
  13. Winek J, Rowinska-Zakrzewska E, Demkow U, et al. Interferon gamma production in the course of Mycobacterium tuberculosis infection. J Physiol Pharmacol. 2008; 59 Suppl 6: 751–759.
  14. Hirsch CS, Toossi Z, Othieno C, et al. Depressed T-cell interferon-gamma responses in pulmonary tuberculosis: analysis of underlying mechanisms and modulation with therapy. J Infect Dis. 1999; 180(6): 2069–2073.
  15. Vankayalapati R, Wizel B, Weis SE, et al. Serum cytokine concentrations do not parallel Mycobacterium tuberculosis-induced cytokine production in patients with tuberculosis. Clin Infect Dis. 2003; 36(1): 24–28.
  16. Sánchez FO, Rodríguez JI, Agudelo G, et al. Immune responsiveness and lymphokine production in patients with tuberculosis and healthy controls. Infect Immun. 1994; 62(12): 5673–5678.
  17. Dlugovitzky D, Bay ML, Rateni L, et al. Influence of disease severity on nitrite and cytokine production by peripheral blood mononuclear cells (PBMC) from patients with pulmonary tuberculosis (TB). Clin Exp Immunol. 2000; 122(3): 343–349.
  18. Fortes A, Pereira K, Antas PRZ, et al. Detection of in vitro interferon-gamma and serum tumour necrosis factor-alpha in multidrug-resistant tuberculosis patients. Clin Exp Immunol. 2005; 141(3): 541–548.
  19. Ferrand RA, Bothamley GH, Whelan A, et al. Interferon-gamma responses to ESAT-6 in tuberculosis patients early into and after anti-tuberculosis treatment. Int J Tuberc Lung Dis. 2005; 9(9): 1034–1039.
  20. Ulrichs T, Anding R, Kaufmann SH, et al. Numbers of IFN-gamma-producing cells against ESAT-6 increase in tuberculosis patients during chemotherapy. Int J Tuberc Lung Dis. 2000; 4(12): 1181–1183.
  21. Verbon A, Juffermans N, Van Deventer SJ, et al. Serum concentrations of cytokines in patients with active tuberculosis (TB) and after treatment. Clin Exp Immunol. 1999; 115(1): 110–113.
  22. Seah GT, Scott GM, Rook GA. Type 2 cytokine gene activation and its relationship to extent of disease in patients with tuberculosis. J Infect Dis. 2000; 181(1): 385–389.

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