Epidermal Compromise in American Cutaneous Leishmaniasis

Abstract

In American cutaneous leishmaniasis (ACL), Leishmania parasites enter the skin of the host via the bite of infected sandflies. Immune Responses Against the parasite vary from "effective" in localized (LCL) to a state of "selective anergy" in diffuse (DCL) cutaneous leishmaniasis, Whereas the intermediate muco-cutaneous form (MCL) is an Exacerbated Characterized by cell-mediated immunity. We Have Shown That in LCL epidermis, Langerhans cells (LC) are Increased, HLA-DR is universally Expressed and intercellular adhesion molecule-1 (ICAM-1) immunoreactivity is distributed in patches. In Addition, mRNA for IL-1 beta, IL-8, TNF alpha, TNF-beta, and gamma INF May be detected in epidermal sheets by reverse transcriptase followed by polymerase chain reaction (RT-PCR). In contrast, LC DCL epidermis shows fewer than LCL epidermis, and expression of ICAM-1, HLA-DR, and IL-1 beta mRNA cannot be detected. MCL injuries show a mucosal epithelium lacking LC, but ICAM-1 is universally Expressed. The clinical manifestations of ACL can be reproduced experimentally in different strains of inbred mice. In healthy mice, We Have shown a positive correlation Between LC and dendritic epidermal T cells (DETC) numbers. This correlation was not, however, Observed in L. Mexican-infected mice, suggesting infection That alters the balance Between the two cell types. In Addition, agents That modulate. LC DETC cell densities and change the development of experimental leishmaniasis These results Suggest That the epidermis is essential in Determining the type of. That immune response is developed Against the Leishmania parasites.