Tissue Damage in Human Cutaneous Leishmaniasis: Correlations Between Inflammatory Cells and Molecule Expression.

Autor:	Saldanha MG; Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Brazil., Pagliari C; Departamento de Patologia, Faculdade de Medicina, Universidade São Paulo, São Paulo, Brazil., Queiroz A; Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Brazil., Machado PRL; Serviço de Imunologia, Complexo Hospitalar Universitário Professor Edgard Santos, Universidade Federal da Bahia, Salvador, Brazil., Carvalho L; Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Brazil.; Serviço de Imunologia, Complexo Hospitalar Universitário Professor Edgard Santos, Universidade Federal da Bahia, Salvador, Brazil., Scott P; Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, United States., Carvalho EM; Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Brazil.; Serviço de Imunologia, Complexo Hospitalar Universitário Professor Edgard Santos, Universidade Federal da Bahia, Salvador, Brazil., Arruda S; Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Brazil.; Departamento de Ciências de Vida, Universidade Estadual da Bahia, Salvador, Brazil.
Jazyk:	angličtina
Zdroj:	Frontiers in cellular and infection microbiology [Front Cell Infect Microbiol] 2020 Jul 14; Vol. 10, pp. 355. Date of Electronic Publication: 2020 Jul 14 (Print Publication: 2020).
DOI:	10.3389/fcimb.2020.00355
Abstrakt:	Cutaneous leishmaniasis (CL) is caused by the bite of the infected sand fly, which inoculates parasites of Leishmania spp and triggers an immune response. An exacerbated cutaneous inflammatory response is crucial for controlling parasite burden but can also promote tissue damage. This study aimed to characterize the populations of natural killer (NK), CD57 + , CD4 + , and CD8 + T cells, CD20 + B cells, as well as CD68 + macrophages, in biopsies of ulcerated CL lesions, and quantify the production of perforin + , grazyme B + , interleukin 1 beta (IL-1β + ) and Tumor Necrosis Factor (TNF-α + cells). We then correlated these parameters with necrosis, inflammation and the number of amastigotes. CD4 + T cells were positively correlated to the extent of inflammation, B cells and IL-1β + were associated with the extent of necrosis, CD68 + macrophages and perforin were correlated with the number of amastigotes, and CD57 + NK cells was correlated to CD68 + macrophages and amastigotes. In sum, the finding suggests that the production of cytotoxic granules and cytokines by inflammatory cells contributes to tissue damage in CL lesions. (Copyright © 2020 Saldanha, Pagliari, Queiroz, Machado, Carvalho, Scott, Carvalho and Arruda.)
Databáze:	MEDLINE
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