Authors: 

Abstract

Introduction: Leprosy remains a public health problem in developing countries. However, the underlying immune mechanism is still poorly understood. In the early non-specific immune protective mechanism, monocyte acts as phagocytes and holds the most significant role. A recent study suggested that IL-10 on APC is might inhibit the expression of MHC-II and co-stimulatory molecules; hence reducing the production of T cells stimulator cytokines.

Method: This observational study was conducted in Makassar, Indonesia, during March to October 2013, with a total of 11 multibacillary (MB) leprosy patients. Samples were collected by consecutive sampling method with the following inclusion criteria; male and female leprosy patients aged 16 – 60 years old, has never been previously treated, and were willing to participate in the study. The patients were treated with WHO multidrug therapy (MDT) and followed up until 3 months after therapy. The monocyte count and IL-10 level were recorded and analysed using Wilcoxon-test.

Results: There was a significant reduction in IL-10 level after treatment (p=0.002). Monocyte count showed increased monocyte level in 7 patients (63.7%) and was found to decrease in 4 subjects (36%). There was no significant difference in mean monocyte count before and after 3 months of MDT-MB WHO therapy (p>0.05).

Conclusion: This study showed that IL-10 level was increased after MDT-MB therapy. Monocyte count was higher after therapy compared to before therapy. There was no relationship between IL-10 level and monocyte count in patients with MB leprosy. Future study should be conducted to examine the monocyte activity in addition to the monocyte count.

 

Citation

 

Keywords

Interleukin-10, Leprosy. Monocyte count, Multibacillary

More Articles

 

/* ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Conditionally display Abstract button ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ */ /* ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Conditionally display References button ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ */