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Tissue Damage in Human Cutaneous Leishmaniasis: Correlations Between Inflammatory Cells and Molecule Expression
Maíra Garcia Saldanha1, Carla Pagliari2, Adriano Queiroz1
1Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Brazil.
Frontiers in Cellular and Infection Microbiology
|August 9, 2020
Summary
Cutaneous leishmaniasis (CL) involves immune cells and inflammatory responses. Inflammatory cell-produced cytotoxic granules and cytokines contribute to tissue damage in CL lesions.
Area of Science:
- Immunology
- Dermatology
- Parasitology
Background:
- Cutaneous leishmaniasis (CL) results from sand fly bites transmitting Leishmania parasites.
- Immune responses control parasite load but can cause tissue damage in CL.
- Characterizing immune cell populations and mediators is key to understanding CL pathology.
Purpose of the Study:
- To analyze immune cell populations (NK, T cells, B cells, macrophages) in CL lesions.
- To quantify cytotoxic molecules (perforin, granzyme B) and cytokines (IL-1β, TNF-α).
- To correlate these immune parameters with lesion characteristics (necrosis, inflammation, parasite load).
Main Methods:
- Biopsies from ulcerated CL lesions were analyzed.
- Flow cytometry and immunohistochemistry were used to identify and quantify cell populations and molecules.
- Statistical correlations were performed between immune parameters and clinical/histopathological findings.
Main Results:
- CD4+ T cells correlated with inflammation.
- B cells and IL-1β+ cells were associated with necrosis.
- CD68+ macrophages and perforin+ cells correlated with amastigote burden.
- CD57+ NK cells correlated with CD68+ macrophages and amastigotes.
Conclusions:
- Immune cell populations and their mediators play a significant role in CL pathogenesis.
- Cytotoxic granule and cytokine production by inflammatory cells contributes to tissue damage in CL.
- Understanding these immune mechanisms can inform future therapeutic strategies for CL.
