Article
Contribution of inflammasome genetics in Plasmodium vivax malaria.
Registro en:
SANTOS, Marina Lima Silva et al. Contribution of inflammasome genetics in Plasmodium vivax malaria. Infect Genet Evol., v. 40, p. 162-6, 2016.
1567-1348
Autor
Santos, Marina Lima Silva
Reis, Edione Cristina
Bricher, Pamela Nithzi
Sousa, Taís Nóbrega de
Brito, Cristiana Ferreira Alves de
Lacerda, Marcus Vinicius Guimaraes de
Fontes, Cor Jesus Fernandes
Carvalho, Luzia Helena de
Pontillo, Alessandra
Resumen
Recent reports showed that, in mice, symptomatic Plasmodium infection triggers NLRP3/NLRP12-dependent inflammasome formation and caspase-1 activation in monocytes. In humans, few works demonstrated that inflammasome is activated in malaria. As Plasmodium vivax is a potent inducer of inflammatory response we hypothesised that inflammasome genetics might affect P. vivax malaria clinical presentation. For this purpose, selected SNPs in inflammasome genes were analysed among patients with symptomatic P. vivax malaria.
157 Brazilian Amazon patients with P. vivax malaria were genotyped for 10 single nucleotide polymorphisms (SNPs) in inflammasome genes NLRP1, NLRP3, AIM2, CARD8, IL1B, IL18 and MEFV. Effect of SNPs on hematologic and clinical parameters was analysed by multivariate analysis.
Our data suggested an important role of NLRP1 inflammasome receptor in shaping the clinical presentation of P. vivax malaria, in termof presence of fever, anaemia and thrombocytopenia. Moreover IL1B rs1143634 resultedsignificantly associated to patients' parasitaemia, while IL18 rs5744256 plays a protective role against the development of anaemia.
Polymorphisms in inflammasome genes could affect one or other aspects of malaria pathogenesis. Moreover, these data reveal novel aspects of P. vivax/host interaction that involved NLRP1-inflammasome. 2021-01-01