The Impact of Thalidomide on Complement Activation by Mycobacterium leprae: An In Vitro Study

Abstract

One inflammatory event that may be involved in erythema nodosum leprosum (ENL) is the activation of complement, 
and thalidomide could suppress ENL by inhibiting its activation. To determine if thalidomide inhibits the activation of 
complement, we first incubated normal serum with Mycobacterium leprae or with zymosan in the presence of 
thalidomide. Residual functional complement was then determined by defining the dilution of the serum required to 
lyses 50% of the rabbit antibody sensitized sheep cells (CH50 Assay). Zymosan and M. leprae activated complement. 
The CH50 values in the serum incubated with M. leprae or with zymosan were equivalent to the CH50 values in the 
serum incubated with M. leprae or zymosan in the presence of thalidomide. Thalidomide did not disrupt the activation 
of complement by zymosan, a know initiator of complement activation by the alternative pathway, or by M. leprae.