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In vitro
thalidomide does not interfere with the activation of
complement by Mycobacterium leprae
E. J. Shannon*, F. G. Sandoval and
M. J. Morales
US Department of Health and Human Services, Health Resources
and Services Administration, National Hansen’s Disease
Programs, Laboratory Research Branch, Louisiana State University,
Baton Rouge, LA, USA.
*Corresponding author. E-mail:
eshann1@lsu.edu. Tel: 225-578-9842.
Accepted 5 March, 2010 |
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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.
Key words:
ENL, thalidomide, complement. |