Inflammation in disseminated lesions: an analysis of CD4+, CD20+, CD68+, CD31+ and vW+ cells in non-ulcerated lesions of disseminated leishmaniasis

Abstract

Disseminated leishmaniasis (DL) differs from other clinical forms of the disease due to the presence of many non-ulcerated lesions (papules and nodules) in non-contiguous areas of the body. We describe the histopathology of DL non-ulcerated lesions and the presence of CD4-, CD20-, CD68-, CD31- and von Willebrand factor (vW)-positive cells in the inflamed area. We analysed eighteen biopsies from non-ulcerated lesions and quantified the inflamed areas and the expression of CD4, CD20, CD68, CD31 and vW using Image-Pro software (Media Cybernetics). Diffuse lymphoplasmacytic perivascular infiltrates were found in dermal skin. Inflammation was observed in 3-73% of the total biopsy area and showed a significant linear correlation with the number of vW + vessels. The most common cells were CD68 + macrophages, CD20 + B-cells and CD4 + T-cells. A significant linear correlation between CD4 + and CD20 + cells and the size of the inflamed area was also found. Our findings show chronic inflammation in all DL non-ulcerated lesions predominantly formed by macrophages, plasmacytes and T and B-cells. As the inflamed area expanded, the number of granulomas and extent of the vascular framework increased. Thus, we demonstrate that vessels may have an important role in the clinical evolution of DL lesions.

American cutaneous leishmaniasis: In situ immune response of patients with recent and late lesions

“…These data suggest that the presence of these two cytokines and CD57 in the early period of infection can be correlated with the control of parasites as previously described in other studies . IFN‐γ synergistically linked to TNF‐α activate macrophages to induce the nitric oxide synthase that leads to death of intracellular parasites . Consequently, both groups of patients expressed similar concentrations of CD68 cells in order to kill amastigotes in infected cells.…”

“…These data suggest an immunological balance between inflammatory‐anti‐inflammatory agents, and such balance was similar for two groups of patients. High expression of IL‐10 at inflamed sites may regulate the host response to tissue damage and lead to later healing . In addition, IL‐10 downregulates IFN‐γ production .…”

“…13,22,[34][35][36][37] IFNγ synergistically linked to TNFα activate macrophages to induce the nitric oxide synthase that leads to death of intracellular parasites. [38][39][40] Consequently, both groups of patients expressed similar concentrations of CD68 cells in order to kill amastigotes in infected cells. However, such cytotoxicity is directly correlated with expressed granzyme causing ulcer development.…”

“…High expression of IL-10 at inflamed sites may regulate the host response to tissue damage and lead to later healing. 13,15,21,40 In addition, IL-10 downregulates IFNγ production. 8,21 The neutralization of IFNγ decreased the production of TNFα.…”

Disseminated Cutaneous Leishmaniasis in a Man With Human Immunodeficiency Virus Infection

“…Cutaneous Leishmais can be visible as an opportunistic infection associated with HIV/AIDS and may be the first symptom in patients with HIV infection in an endemic area (2-5, 8, 9). In 2013, a relationship between disseminated CL and CD4 count was reported by Mendes et al (6). They showed that chronic inflammations in all DCL non-ulcerated lesions are predominantly formed by macrophages, plasmacytes, and T-and B-cells.…”