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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Involvement of the Inflammasome and Th17 Cells in Skin Lesions of Human Cutaneous Leishmaniasis Caused by Leishmania (Viannia) panamensis

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Gonzalez, K. [1, 2] ; Calzada, J. E. [1, 3] ; Corbett, C. E. P. [2] ; Saldana, A. [1, 4] ; Laurenti, M. D. [2]
Total Authors: 5
[1] Inst Conmemorativo Gorgas Estudios Salud, Dept Parasitol Mol, Av. Justo Arosemena, Panama City 081602593 - Panama
[2] Univ Sao Paulo, Lab Patol Molestias Infecciosas, Fac Med, Dept Patol, Ave Doutor Arnaldo 455, BR-01246903 Sao Paulo, Cerqueira Cesar - Brazil
[3] Univ Panama, Fac Med Vet, Campus Harmodio Arias Madrid, Av Juan Pablo II, Panama City - Panama
[4] Univ Panama, Ctr Invest & Diagnost Enfermedades Parasitarias, Fac Med, Ave Octavio Mendez Pereira, Panama City - Panama
Total Affiliations: 4
Document type: Journal article
Source: Mediators of Inflammation; v. 2020, OCT 28 2020.
Web of Science Citations: 0

Localized cutaneous leishmaniasis (LCL) caused by Leishmania (Viannia) panamensis is an endemic disease in Panama. This condition causes ulcerated skin lesions characterized by a mixed Th1/Th2 immune response that is responsible for disease pathology. However, the maintenance of the in situ inflammatory process involves other elements, such as Th17 and inflammasome responses. Although these processes are associated with parasite elimination, their role in the increase in disease pathology cannot be discarded. Thus, the role in Leishmania infection is still unclear. In this sense, the present study aimed at characterizing the Th17 and inflammasome responses in the skin lesions of patients with LCL caused by L. (V.) panamensis to help elucidate the pathogenesis of this disease in Panama. Th17 and inflammasome responses were evaluated by immunohistochemistry (IHQ) in 46 skin biopsies from patients with LCL caused by L. (V.) panamensis. The Th17 immune response was assessed using CD3, CD4, RoR gamma t, IL-17, IL-6, IL-23, and TGF-beta 1 antibodies, and the inflammasome response was assessed by IL-1 beta, IL-18, and caspase-1 antibodies. The presence of the Th17 and inflammasome responses was evidenced by a positive reaction for all immunological markers in the skin lesions. An inverse correlation between the density of amastigotes and the density of RoR gamma t(+), IL-17(+), IL-1 beta(+), and caspase-1(+) cells was observed, but no correlation between Th17 and the inflammasome response with evolutionary disease pathology was reported. These data showed the participation of Th17 cells and the inflammasome in the inflammatory response of the skin lesions of LCL caused by L. (V.) panamensis infection. These results suggest a role in the control of tissue parasitism of IL-17 and the activation of the NLRP3 inflammasome dependent on IL-1 beta but cannot exclude their role in the development of disease pathology. (AU)

FAPESP's process: 17/03141-5 - Characterization of histopathological changes and cellular immune response in cutaneous lesions of patients with Tegumentary Leishmaniasis in Panamá
Grantee:Kadir Amilcar Gonzalez Carrion
Support type: Scholarships in Brazil - Doctorate (Direct)
FAPESP's process: 14/50315-0 - Leishmaniasis in Latin America: an advanced perspective on immunopathogenetic factors of cutaneous and visceral infection, immunomodulators of the sandflies vector saliva and immunogenic exo-antigens of Leishmania (L.) infantum chagasi as vaccine candidates
Grantee:Carlos Eduardo Pereira Corbett
Support type: Research Projects - Thematic Grants