INTRODUCTION
Leprosy is a chronic granulomatous disease caused by mycobacterium leprae (M. Leprae) with a specific predilection to cutaneous and neural tissue. Immunologic and inflammatory changes result in a wide range of skin and nerve tissue manifestations that end up with neural destruction and physical impairments.1
The concentration and adhesion of M. Leprae to the extracellular matrix of Schwann cells can result in irreversible damage of neural tissue and consequently in nerve functions. It is therefore of utmost importance to identify and early treat leprotic affections to limit significant disabilities.2
Anti-neural antibodies are known to play a role in the immunopathogenesis of nerve damage in leprosy. Ceramide is a glycosphingolipid that is expressed as a surface determinant of myelin. Antibodies to ceramide or related neural components of the myelin sheath may be associated with extensive nerve damage.3
Multibacillary leprosy (MB) (Lepromatous) is Th2 mediated condition as opposed to paucibacillary leprosy (PB) which is a Th1 predominately mediated condition. In multibacillary leprosy, there is an inhibition of IL-12 signals as well as the increased response of IL-4 with subsequent disease progression.4
In MB leprosy patients, both IL-4 and anti-ceramide antibody titres increase, however, the mechanisms by which the cellular immune response and the whole spectrum of cytokine release remains to be fully elucidated.5
The present study aimed to evaluate IL-4 and antibodies to ceramide in the sera of leprosy patients and healthy subjects using enzyme linked immunosorbent assay (ELISA) to determine their possible role and correlation of their severity in nerve damage.
The concentration and adhesion of M. Leprae to the extracellular matrix of Schwann cells can result in irreversible damage of neural tissue and consequently in nerve functions. It is therefore of utmost importance to identify and early treat leprotic affections to limit significant disabilities.2
Anti-neural antibodies are known to play a role in the immunopathogenesis of nerve damage in leprosy. Ceramide is a glycosphingolipid that is expressed as a surface determinant of myelin. Antibodies to ceramide or related neural components of the myelin sheath may be associated with extensive nerve damage.3
Multibacillary leprosy (MB) (Lepromatous) is Th2 mediated condition as opposed to paucibacillary leprosy (PB) which is a Th1 predominately mediated condition. In multibacillary leprosy, there is an inhibition of IL-12 signals as well as the increased response of IL-4 with subsequent disease progression.4
In MB leprosy patients, both IL-4 and anti-ceramide antibody titres increase, however, the mechanisms by which the cellular immune response and the whole spectrum of cytokine release remains to be fully elucidated.5
The present study aimed to evaluate IL-4 and antibodies to ceramide in the sera of leprosy patients and healthy subjects using enzyme linked immunosorbent assay (ELISA) to determine their possible role and correlation of their severity in nerve damage.