Production of cytokines in patients with primary pulmonary Mycobacterium avium-intracellulare complex disease.

To clarify the immunological state of patients with pulmonary Mycobacterium avium-intracellulare complex (MAC) disease, we compared the production of IFN-gamma, IL-10 and TNF-alpha by peripheral blood mononuclear cells (PBMC) between MAC disease patients with different levels of disease activity and healthy volunteers. The patients had no complication of systemic immunological diseases or preexisting pulmonary diseases. PBMC obtained from 46 patients and 15 healthy control volunteers were incubated with a protein antigen extracted from Mycobacterium intracellulare (PPD-B) for seven days, and IFN-gamma, IL-10 and TNF-alpha concentration in the supernatant of the cultures was measured by enzyme-linked immunosorbent assay (ELISA). We categorized the patients into 3 groups based on the findings of chest radiography or results of sputum culture for MAC: group I in a stable state of the disease activity (15 patients), group II in an unstable state (16 patients) and group III in an active state of the disease (15 patients). IFN-gamma was low in all three patient groups compared to the healthy group. There was no difference of the concentration of IFN-gamma among the three patient groups. IL-10 was high in the patient groups compared to the healthy group, and the concentration of IL-10 in the patients of groups II and III was significantly higher than in the healthy group. Although the production of TNF-alpha in group I was significantly suppressed compared to the healthy group, the production of TNF-alpha was significantly elevated in groups II and III compared to group I. There was no difference in the production of these cytokines between the patients of group III with tuberculosis-like form and with nodular-bronchietasis form. These findings suggested that the Th1-type reaction in the patients with primary pulmonary MAC disease is suppressed (lower than the healthy persons) irrespective of the disease activity state and that the Th2-type reaction is increased in parallel with disease activity.