Abstract
IntroductionCutaneous leishmaniasis (CL) due to L.braziliensis infection is characterized by a strong inflammatory response with high levels of TNF and ulcer development. Less attention has been given to the role of mononuclear phagocytes to this process. Monocytes constitute a heterogeneous population subdivided into classical, intermediate and non-classical, and are known to migrate to inflammatory sites and secrete inflammatory mediators. TNF participates in the induction of matrix metalloproteinases (MMPs). MMP-9 is an enzyme that degrades basal membrane and its activity is controlled by the tissue inhibitor of metalloproteinase.MethodsMononuclear cells were obtained from ex-vivo labeling sub-populations of monocytes and MMP-9, and the frequency was determined by flow cytometry. Culture was performed during 72 hours, stimulating the cells with SLA, levels of MMP-9 and TIMP-1 in the supernatants were determined by ELISA.ResultsWe observed that cells from CL lesions secrete high amounts of MMP-9 when compared to healthy subjects. Although MMP-9 was produced by monocytes, non-classical ones were the main source of this enzyme. We also observed that TNF produced in high level during CL contributes to MMP-9 production.ConclusionsThese observations emphasize the role of monocytes, TNF and MMP-9 in the pathogenesis of L. braziliensis infection.
Highlights
Cutaneous leishmaniasis (CL) due to L.braziliensis infection is characterized by a strong inflammatory response with high levels of TNF and ulcer development
matrix metalloproteinases (MMPs)-9 was produced by monocytes, non-classical ones were the main source of this enzyme
These observations emphasize the role of monocytes, TNF and MMP-9 in the pathogenesis of L. braziliensis infection
Summary
Cutaneous leishmaniasis (CL) due to L.braziliensis infection is characterized by a strong inflammatory response with high levels of TNF and ulcer development. Most patients develop lymphadenopathy, followed by the appearance of a papule at the bite site, which subsequently becomes an ulcerated lesion These lesions are composed of a robust inflammatory infiltrate including the presence of T and B lymphocytes, mononuclear phagocytes and plasma cells [2]. During L. braziliensis infection these cells are activated and TNF and IFN-c are produced in high levels both by peripheral blood mononuclear cells (PBMC) and at lesion site of CL patients. This response can lead to tissue damage and development of the ulcer [4]
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