Inflammasome gene expression is associated with immunopathology in human localized cutaneous leishmaniasis

Autor(es):Mostrar menos -

Gupta, Gaurav ^{[1, 2]} ; Santana, Alynne K. M. ^[1] ; Gomes, Ciro M. ^[3] ; Turatti, Aline ^[4] ; Milanezi, Cristiane M. ^[1] ; Bueno Filho, Roberto ^[4] ; Fuzo, Carlos ^[1] ; Almeida, Roque P. ^[5] ; Carregaro, Vanessa ^[1] ; Roselino, Ana M. ^[4] ; Silva, Joao S. ^{[1, 6]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Dept Biochem & Immunol, Bandeirantes Ave 3900, BR-14049900 Ribeirao Preto - Brazil

^[2] Univ Manitoba, Dept Immunol, Winnipeg, MB - Canada

^[3] Univ Brasilia, Fac Med, Dept Med Clin, Div Dermatol, Brasilia, DF - Brazil

^[4] Univ Sao Paulo, Fac Med, Dept Med Clin, Div Dermatol, Sao Paulo - Brazil

^[5] Univ Fed Sergipe, Dept Med, Aracaju - Brazil

^[6] Fiocruz MS, Fundacao Oswaldo Cruz, Biinst Translat Med Project, Rio De Janeiro - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Cellular Immunology; v. 341, JUL 2019.
• Citações Web of Science: 1

Resumo

Localized cutaneous leishmaniasis (LCL) can ultimately progress to chronic ulcerated lesions with strong local inflammatory reactions. The functional role of certain inflammasomes in mediating inflammation caused by Leishmania braziliensis needs to be addressed. By combining PCR-array, quantitative real-time PCR and immunohistochemical analysis, we identified inflammasome genes, such as IL-1 beta, NLRP3, NLRP1, NLRC5, AIM2 and P2RX7, that were upregulated in LCL patients. Temporal gene expression studies showed that the early phase of LCL displayed increased NLRP3 and reduced AIM2 and NLRP1 expression, while the late stages showed increased AIM2 and NLRP1 and lower NLRP3 expression. Our findings also showed that AIM2, NLRP1, and P2RX7 promoted susceptibility to experimental L. braziliensis infection. These results highlight the importance of inflammasome machinery in human LCL and suggest that inflammasome machinery plays a role in the acute and chronic phases of the disease. (AU)

• Processo FAPESP: 13/08216-2 - CPDI - Centro de Pesquisa em Doenças Inflamatórias
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs