Dominant Th1 Cytokine Production in Early Onset of Human Brucellosis Followed by Switching Towards Th2 Along Prolongation of Disease

J Infect. 2006 Nov;53(5):315-24. doi: 10.1016/j.jinf.2005.11.024. Epub 2006 Feb 20.

Abstract

Human brucellosis is a worldwide zoonotic infectious disease which is caused by intracellular bacteria belonging to the genus Brucella. Based on murine studies it has been shown that host resistance to Brucella depends on Th1 response, whereas Th2 response is involved in the severity of the disease. Since the immune response during human brucellosis has not been profoundly studied we have tried to evaluate cytokine production in patients suffering from brucellosis. Diluted whole blood samples were cultured in the presence of the mitogen, heat inactivated bacteria or medium alone. IL-12, IFN-gamma and IL-10 were measured by specific sandwich ELISA. In addition, the percentage of CD3(+) T cells producing either IL-13 or IFN-gamma was determined by flow cytometry. It was found that not only IFN-gamma production but also the number of CD3(+) IFN-gamma-producing cells decreased with prolongation of the disease but the percentage of CD3(+) IL-13(+) T cells were significantly increased. No correlation between duration of disease and IL-10 or IL-12 production was found. In conclusion, it is proposed that at the onset of brucellosis, Th1 response dominates while diminishing with prolongation of the disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Brucellosis / immunology*
  • CD3 Complex / immunology
  • Cytokines / biosynthesis*
  • Cytokines / immunology
  • Disease Progression
  • Down-Regulation
  • Female
  • Humans
  • Interferon-gamma / immunology
  • Interleukin-10 / immunology
  • Interleukin-12 / immunology
  • Interleukin-13 / immunology
  • Lymphocyte Activation
  • Male
  • Middle Aged
  • Th1 Cells / immunology*
  • Th2 Cells / immunology*

Substances

  • CD3 Complex
  • Cytokines
  • Interleukin-13
  • Interleukin-10
  • Interleukin-12
  • Interferon-gamma