title: [The relation between diabetes mellitus and IFN-gamma, IL-12 and IL-10 productions by CD4+ alpha beta T cells and monocytes in patients with pulmonary tuberculosis].
abstract: Diabetics are prone to bacterial infection in part, due to polymorphonuclear neutrophil dysfunction, but the precise mechanism is not yet fully explained. Of many complications, diabetes mellitus (DM) is one of the most common diseases, which causes pulmonary tuberculosis. To elucidate the mechanism of susceptibility to tuberculosis infection in patients with diabetes mellitus, we measured IFN-gamma, IL-12 and IL-10 productions by CD4+ alpha beta T cells and autologous monocytes stimulated with live BCG in patients with pulmonary tuberculosis complicated with DM (TB + DM) or without DM (TB) and healthy controls. The levels of IFN-gamma and IL-12 production in TB patients were significantly lower than those in the control. These cytokine productions were also lower in TB + DM patients than in TB patients significantly. The level of IL-10 production in TB patients were highest among these three groups. The production of this cytokine in TB + DM patients was lowest. The level of IFN-gamma production was significantly lower in TB + DM patients under poor DM control than in those patients under good DM control and showed a significant negative correlation to HbA1c, an indicator of diabetic control. The period for negative conversion of culture finding in TB + DM patients under poor control was prolonged when compared with those in TB patients. These results demonstrated the difference in cytokines secretion profile between TB patients and TB + DM patients, and suggest that the immunological mechanism underlying pathogenesis of tuberculosis might work differently between these two patients groups.
authors.affiliation: Second Department of Internal Medicine, Nara Medical University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Tsukaguchi
authors.forename: H
authors.initials: H
authors.lastname: Okamura
authors.forename: M
authors.initials: M
authors.lastname: Ikuno
authors.forename: A
authors.initials: A
authors.lastname: Kobayashi
authors.forename: A
authors.initials: A
authors.lastname: Fukuoka
authors.forename: H
authors.initials: H
authors.lastname: Takenaka
authors.forename: C
authors.initials: C
authors.lastname: Yamamoto
authors.forename: T
authors.initials: T
authors.lastname: Tokuyama
authors.forename: Y
authors.initials: Y
authors.lastname: Okamoto
authors.forename: A
authors.initials: A
authors.lastname: Fu
authors.forename: M
authors.initials: M
authors.lastname: Yoshikawa
authors.forename: T
authors.initials: T
authors.lastname: Yoneda
authors.forename: N
authors.initials: N
authors.lastname: Narita
mesh_terms: D000328:Adult; D000368:Aged; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000276:immunology*; D004198:Disease Susceptibility; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis*; D016753:Interleukin-10 / Q000096:biosynthesis*; D018664:Interleukin-12 / Q000096:biosynthesis*; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism; D014397:Tuberculosis, Pulmonary / Q000209:etiology* / Q000276:immunology
chemical_list: D016753:Interleukin-10; D018664:Interleukin-12; D007371:Interferon-gamma