Role of calcium channels in cellular antituberculosis effects: Potential of voltage-gated calcium-channel blockers in tuberculosis therapy
Lele Song, Ruina Cui, Yourong Yang, Xueqiong Wu
Received: April 30, 2014 Revised: June 13, 2014 Accepted: August 7, 2014
Xueqiong Wu, Corresponding author. Army Tuberculosis Prevention and Control Key Laboratory, Institute of Tuberculosis Research, The 309th Hospital of Chinese PLA, No. 17, Heishanhu Road, Haidian District, Beijing 100091, China.
Background and purpose:
The immunity of human immune cells and their ability to inhibit Mycobacterium tuberculosis (MTB) are key factors in the anti-MTB effect. However, MTB modulates the levels and activity of key intracellular second messengers, such as calcium, to evade protective immune responses. Recent studies suggest that inhibiting L-type calcium channel in immune cells using either antibodies or small interfering RNA increases calcium influx, upregulates the expression of proinflammation genes, and reduces MTB burden. First, we will review the key factors in calcium-signaling pathway that may affect the immunity of immune cells to MTB infection. Second, we will focus on the role of calcium channels in regulating cellular immunity to MTB. Finally, we will discuss the possibility of using calcium-channel blockers as anti-MTB chemotherapy drugs to enhance chemotherapy effects, shorten treatment period, and overcome drug resistance.
calcium channel, calcium signaling, immunity, Mycobacterium tuberculosis