Wu H-P, Hua C-C, Liu Y-C, Chuang D-Y
Division of Pulmonary Medicine, Department of Internal Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan, No. 222, Maijin Road, Anle Chiu, Keelung 204, Taiwan, ROC.
Inflamm Res. 2007 Jan;56(1):11-6. doi: 10.1007/s00011-007-6083-9.
Macrophages aided by interferon-gamma (IFN-gamma) are vital to controlling Mycobacterium tuberculosis (M. tuberculosis) infection. Although numerous studies have compared IFN-gamma response between tubercular patients and healthy controls, no studies have investigated IFN-gamma response in patients with pulmonary tuberculosis and non-tubercular pneumonia. The aim of this work was to examine the difference in IFN-gamma response between patients with tuberculosis and non-tubercular pneumonia.
IFN-gamma production was detected based on the difference in supernatants between non-stimulated and stimulated peripheral blood mononuclear cells by phytohemagglutinin in 83 tubercular patients and 47 patients with pneumonia. Presence of a cavity on chest radiography and co-morbidities of pneumoconiosis, bronchiectasis, liver cirrhosis, renal failure on hemodialysis, diabetes mellitus (DM) and lung cancer were recorded for analysis.
Interferon-gamma response, DM and a cavity on chest radiography were independent factors for predicting active pulmonary tuberculosis. Interferon-gamma response was decreased in patients with pulmonary tuberculosis compared with that in patients with non-tubercular pneumonia. Notably, M. tuberculosis infection was the principal factor correlated with IFN-gamma response.
The IFN-gamma response was principally affected by M. tuberculosis infection and not by other co-morbidities. Further study is required to identify the mechanism of decreased IFN-gamma production.