Differential expression of solute carrier family 11a member 1 and inducible nitric oxide synthase 2 in skin biopsies from leprosy patients.
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Date
2015-11
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Abstract
Background: Leprosy is a chronic granulomatous infection caused by Mycobacterium leprae,
an intracellular parasite that resides within macrophages and cannot be eliminated effectively.
Solute carrier family 11a member 1 (Slc11a1) and inducible nitric oxide synthase (iNOS),
both expressed in macrophages, play major roles in host defense against several intracellular
pathogens. However, the roles of these molecules in natural infection with M. leprae remain
unknown. Objective: We aimed to investigate the expression of Slc11a1 and iNOS in
macrophages (CD68+ cells) infi ltrating skin lesions in leprosy. Methods: Skin biopsies from
48 Mexican patients of leprosy [(33 lepromatous (LL), 15 tuberculoid (TT)] and from 10 healthy
controls, were subjected to immunohistochemistry to determine expression of CD68, Slc11a1
and iNOS. Results: We found a high expression of Slc11a1 and iNOS in most lepromatous
leprosy samples. In tuberculoid leprosy samples, Slc11a1 expression was moderate or low,
and that of iNOS was almost always low. In addition, Slc11a1 and iNOS expression levels
were positively associated with bacillary loads in lepromatous leprosy lesions (P = 0.05).
Conclusions: These observations suggest that M. leprae infection promotes the expression
of Slc11a1 and iNOS in macrophages and that lepromatous leprosy can occur despite this
response.
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Keywords
Immune response, macrophage, solute carrier family 11a member 1, inducible nitric oxide synthase, leprosy, lepromatous, tuberculoid, Slc11a1, NRAMP1, iNOS
Citation
Pereira-Suárez Ana Laura, Alvarado-Navarro Anabell, Barrietos-García Juan Gabriel, Estrada-Chávez Ciro, Muñoz-Valle José Francisco, Fafutis-Morris Mary. Differential expression of solute carrier family 11a member 1 and inducible nitric oxide synthase 2 in skin biopsies from leprosy patients. Indian Journal of Dermatology, Venereology and Leprology. 2015 Nov-Dec; 81(6): 594-599.