A Study of The Role of IL-12 in Pulmonary Tuberculosis Using the Whole Blood Flowcytometry Technique

¹Wafaa A. Zahran, ¹Mabrouk M. Ghonaim, ¹Bothina A. Koura, ¹Hassan El-Banna, ¹Sahar M. Ali and ²Nabila El-Sheikh

¹Microbiology & Immunology department, Faculty of Medicine, Menofiya University, and ²Microbiology department, Faculty of Medicine for Girls, Al-Azhar University, Egypt.

Pulmonary tuberculosis remains a major health problem. It is caused by Mycobacterium tuberculosis, which elicits a T-cell dependent immune response, initiated by monocytes through a large number of cytokines of which interleukin-12 is thought to play a critical role in initiation and regulation of T-helper (Th-1) like responses. To better understand the role of IL-12 in pulmonary tuberculosis patients, intracellular IL-12 in peripheral blood-derived monocytes was examined by flowcytometery. The percentage of monocytes producing IL-12 was measured after invitro stimulation of heparinized whole blood with mycobacterial protein antigens (culture filtrate). Of the 22 active tuberculosis patients, 17 were recent cases and 5 recurrent cases. Healthy controls were 14 individuals with detectable reaction to purified protein derivative (PPD+) and 14 without detectable reaction to PPD. The role of different factors affecting disease outcome such as treatment, age, gender, smoking, severity of disease and presence of other complications on the percentage of monocytes producing IL-12 was studied. Recurrent TB patients had a higher number of monocytes producing IL-12 in unstimulated cultures compared to other groups (P<0.001). However, after in vitro stimulation there was a significant decrease in the number of monocytes producing IL-12 in recurrent TB patients as compared to recently diagnosed TB patients and healthy PPD⁺ individuals (P<0.001). Antituberculosis chemotherapy was the only factor that had significant effect on the percentage of monocytes producing IL-12 (p< 0.05) while other studied factors did not show significant effect (p>0.05). It is concluded that IL-12 plays a prominent regulatory role in tuberculosis.