As patients with diabetes mellitus are at increased risk of developing tuberculosis, we hypothesized that this susceptibility to mycobacterial infection is due to a defective Th1-cytokine response. To explore this hypothesis, we examined four groups of subjects in Indonesia: 23 patients with tuberculosis, 34 patients with tuberculosis and diabetes, 32 patients with diabetes only and 36 healthy controls. Ex-vivo production of interferon (IFN)γ, tumour necrosis factor-α and interleukin (IL)-1β, 6, 10, -12 and -4 was measured following stimulation with Mycobacterium tuberculosis, Escherichia coli lipopolysaccharide and phytohaemagglutinin. Patients with active tuberculosis were found to have lower IFNγ levels and a higher production of other pro-inflammatory cytokines and IL-4, both in the presence and absence of diabetes. Diabetes patients without tuberculosis, however, showed strongly reduced non-specific IFNγ production, which is essential for inhibition of the initial growth of M. tuberculosis. Our data suggest that a defective non-specific immune response in diabetes may contribute to an increased susceptibility to develop tuberculosis. © 2007 Springer-Verlag.
CITATION STYLE
Stalenhoef, J. E., Alisjahbana, B., Nelwan, E. J., Van Der Ven-Jongekrijg, J., Ottenhoff, T. H. M., Van Der Meer, J. W. M., … Van Crevel, R. (2008). The role of interferon-gamma in the increased tuberculosis risk in type 2 diabetes mellitus. European Journal of Clinical Microbiology and Infectious Diseases, 27(2), 97–103. https://doi.org/10.1007/s10096-007-0395-0
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