Franciele Maira Moreira Batista Tomaz1, Adriana Antônia da Cruz Furini2, Marcela Petrolini Capobianco3, Marinete Marins Póvoa4, Pamella Cristina Alves Trindade5, Valéria Daltibari Fraga6, Luciana Moran Conceição7, Lucas Ribeiro de Azevedo8, Sônia Maria Oliani9, Gustavo Capatti Cassiano10, Carlos Eugênio Cavasini11, Sidney Emanuel Batista Dos Santos12, Ricardo Luiz Dantas Machado13. 1. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil. Electronic address: mairabiomed@hotmail.com. 2. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil. Electronic address: adriana.cruz.furini@gmail.com. 3. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil; Júlio de Mesquita Filho, Universidade Estadual Paulista, São José do Rio Preto, São Paulo State, Brazil. Electronic address: mpcapobianco@yahoo.com.br. 4. Evandro Chagas Institute, MS/SVS, Ananindeua, Pará, Brazil. Electronic address: povoamm@gmail.com. 5. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil. Electronic address: pamella.trindade@hotmail.com. 6. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil. Electronic address: valeriafraga@famerp.br. 7. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil. Electronic address: lucianamoran@famerp.br. 8. Júlio de Mesquita Filho, Universidade Estadual Paulista, São José do Rio Preto, São Paulo State, Brazil. Electronic address: azevedolucasr@gmail.com. 9. Júlio de Mesquita Filho, Universidade Estadual Paulista, São José do Rio Preto, São Paulo State, Brazil. Electronic address: smoliani@ibilce.unesp.br. 10. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil; Júlio de Mesquita Filho, Universidade Estadual Paulista, São José do Rio Preto, São Paulo State, Brazil. Electronic address: gcapatti@hotmail.com. 11. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil. Electronic address: cecavasini@famerp.br. 12. Federal University of Pará, Institute of Biological Sciences, Belém, Pará, Brazil. Electronic address: sidneysantos@ufpa.br. 13. Microorganism Research Center, Department of Dermatological, Infectious, and Parasitic Diseases, Faculdade de Medicina de São José do Rio Preto, São Paulo, Brazil; Júlio de Mesquita Filho, Universidade Estadual Paulista, São José do Rio Preto, São Paulo State, Brazil; Evandro Chagas Institute, MS/SVS, Ananindeua, Pará, Brazil. Electronic address: ricardomachado@iec.pa.gov.br.
Abstract
BACKGROUND: Several studies have recently demonstrated that the immune responses against malaria is governed by different factors, including the genetic components of the host. The IL-4 gene appears to be a strong candidate factor because of its role in the regulation of the Th2 response. The present study investigated the role of IL-4 polymorphisms in the development of IgG antibodies against PvAMA-1 and the IL-4 levels in individuals infected with Plasmodium vivax in a malaria endemic area in the Brazilian Amazon. METHODS: The study sample included 83 patients who were diagnosed with P. vivax infection using thick smear and confirmed by nested-PCR. The IL-4 -590C>T and IL-4 -33C>T polymorphisms were genotyped by PCR-RFLP, and the intron 3 VNTR was genotyped by PCR. A standardised ELISA protocol was used to measure the total IgG against PvAMA-1. The cytokine/chemokine levels were measured using a Milliplex multiplex assay (Millipore). All of the subjects were genotyped with 48 ancestry informative markers to determine the proportions of African, European and Amerindian ancestry using STRUCTURE software. RESULTS: Of the 83 patients, 60 (73%) produced IgG antibodies against PvAMA-1. A significant decrease in the percentage of respondents was observed among the primo-infected individuals. No significant differences were observed in the frequencies of genotypes and haplotypes among individuals who were positive or negative for IgG antibodies against PvAMA-1. Furthermore, no significant correlation was observed between the IL-4 polymorphisms, antibody levels, IL-4 levels, and parasitemia. CONCLUSIONS: This study indicated that the polymorphisms identified in the IL-4 gene are not likely to play a role in the regulation of the antibody response against PvAMA-1 and IL-4 production in vivax malaria.
BACKGROUND: Several studies have recently demonstrated that the immune responses against malaria is governed by different factors, including the genetic components of the host. The IL-4 gene appears to be a strong candidate factor because of its role in the regulation of the Th2 response. The present study investigated the role of IL-4 polymorphisms in the development of IgG antibodies against PvAMA-1 and the IL-4 levels in individuals infected with Plasmodium vivax in a malaria endemic area in the Brazilian Amazon. METHODS: The study sample included 83 patients who were diagnosed with P. vivaxinfection using thick smear and confirmed by nested-PCR. The IL-4 -590C>T and IL-4 -33C>T polymorphisms were genotyped by PCR-RFLP, and the intron 3 VNTR was genotyped by PCR. A standardised ELISA protocol was used to measure the total IgG against PvAMA-1. The cytokine/chemokine levels were measured using a Milliplex multiplex assay (Millipore). All of the subjects were genotyped with 48 ancestry informative markers to determine the proportions of African, European and Amerindian ancestry using STRUCTURE software. RESULTS: Of the 83 patients, 60 (73%) produced IgG antibodies against PvAMA-1. A significant decrease in the percentage of respondents was observed among the primo-infected individuals. No significant differences were observed in the frequencies of genotypes and haplotypes among individuals who were positive or negative for IgG antibodies against PvAMA-1. Furthermore, no significant correlation was observed between the IL-4 polymorphisms, antibody levels, IL-4 levels, and parasitemia. CONCLUSIONS: This study indicated that the polymorphisms identified in the IL-4 gene are not likely to play a role in the regulation of the antibody response against PvAMA-1 and IL-4 production in vivax malaria.
Authors: Adriana A C Furini; Marcela P Capobianco; Luciane M Storti-Melo; Maristela G Cunha; Gustavo C Cassiano; Ricardo Luiz D Machado Journal: Malar J Date: 2016-07-19 Impact factor: 2.979
Authors: Camilla V Pires; Jessica R S Alves; Barbara A S Lima; Ruth B Paula; Helena L Costa; Leticia M Torres; Taís N Sousa; Irene S Soares; Bruno A M Sanchez; Cor J F Fontes; Francis B Ntumngia; John H Adams; Flora S Kano; Luzia H Carvalho Journal: PLoS One Date: 2018-11-12 Impact factor: 3.240
Authors: Camila M P Medeiros; Eduardo U M Moreira; Camilla V Pires; Letícia M Torres; Luiz F F Guimarães; Jéssica R S Alves; Bárbara A S Lima; Cor J F Fontes; Helena L Costa; Cristiana F A Brito; Tais N Sousa; Francis B Ntumngia; John H Adams; Flora S Kano; Luzia H Carvalho Journal: PLoS One Date: 2020-05-07 Impact factor: 3.240