Browsing by Author "Baia-da-Silva, Djane Clarys"
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Item Plasmodium vivax Gametocytes Adherence to Bone Marrow Endothelial Cells(2021) Salazar Alvarez, Luis Carlos; Vera Lizcano, Omaira; da Silva Barros, Dayanne Kamylla Alves; Baia-da-Silva, Djane Clarys; Monteiro, Wuelton Marcelo; Pimenta, Paulo Filemon Paolluci; de Lacerda, Marcus Vinicius Guimarães; Costa, Fabio Trindade Maranhão; Lopes, Stefanie Costa PintoIn a Plasmodium vivax infection, it was shown a proportionally increased on gametocyte distribution within the bone marrow aspirant, suggesting a role of this organ as a reservoir for this parasite stage. Here, we evaluated the ex vivo cytoadhesive capacity of P. vivax gametocytes to bone marrow endothelial cells (HBMEC) and investigated the involvement of some receptors in the cytoadhesion process by using transfected CHO cells (CHO-ICAM1, CHO-CD36 and CHO-VCAM), wild type (CHO-K1) or deficient in heparan and chondroitin sulfate (CHO-745). Ex-vivo cytoadhesion assays were performed using a total of 44 P. vivax isolates enriched in gametocyte stages by Percoll gradient in the different cell lines. The majority of isolates (88.9%) were able to adhere to HBMEC monolayer. ICAM1 seemed to be the sole receptor significantly involved. CD-36 was the receptor with higher adhesion rate, despite no significance was noticed when compared to CHO-745. We demonstrated that gametocyte P. vivax adheres ex vivo to bone marrow endothelial cells. Moreover, P. vivax gametocytes display the ability to adhere to all CHO cells investigated, especially to CHO-ICAM1. These findings bring insights to the comprehension of the role of the bone marrow as a P. vivax reservoir and the potential impact on parasite transmission to the vectorItem The role of the peritrophic matrix and red blood cell concentration in Plasmodium vivax infection of Anopheles aquasalis.(Parasites and Vectors, 2018) Baia-da-Silva, Djane Clarys; Salazar Alvarez, Luis Carlos; Vera Lizcano, Omaira; Maranhão Costa, Fabio Trindade; Costa Pinto Lopes, Stefanie; Silva Orfanó, Alessandra; Oliveira Pascoal, Denner; Nacif-Pimenta, Rafael; Cabral Rodriguez, Iria; Barbosa Guerra, Maria das Graças Vale; Guimarães Lacerda, Marcus Vinicius; Costa Secundino, Nagila Francinete; Monteiro, Wuelton Marcelo; Paolucci Pimenta, Paulo FilemonBackground: Plasmodium vivax is predominant in the Amazon region, and enhanced knowledge of its development inside a natural vector, Anopheles aquasalis, is critical for future strategies aimed at blocking parasite development. The peritrophic matrix (PM), a chitinous layer produced by the mosquito midgut in response to blood ingestion, is a protective barrier against pathogens. Plasmodium can only complete its life-cycle, and consequently be transmitted to a new host, after successfully passing this barrier. Interestingly, fully engorged mosquitoes that had a complete blood meal form a thicker, well-developed PM than ones that feed in small amounts. The amount of red blood cells (RBC) in the blood meal directly influences the production of digestive enzymes and can protect parasites from being killed during the meal digestion. A specific study interrupting the development of the PM associated with the proteolytic activity inhibition, and distinct RBC concentrations, during the P. vivax infection of the New World malaria vector An. aquasalis is expected to clarify whether these factors affect the parasite development. Results: Absence of PM in the vector caused a significant reduction in P. vivax infection. However, the association of chitinase with trypsin inhibitor restored infection rates to those of mosquitoes with a structured PM. Also, only the ingestion of trypsin inhibitor by non-chitinase treated mosquitoes increased the infection intensity. Moreover, the RBC concentration in the infected P. vivax blood meal directly influenced the infection rate and its intensity. A straight correlation was observed between RBC concentrations and infection intensity. Conclusions: This study established that there is a balance between the PM role, RBC concentration and digestive enzyme activity influencing the establishment and development of P. vivax infection inside An. aquasalis. Our results indicate that the absence of PM in the midgut facilitates digestive enzyme dispersion throughout the blood meal, causing direct damage to P. vivax. On the other hand, high RBC concentrations support a better and thick, well-developed PM and protect P. vivax from being killed. Further studies of this complex system may provide insights into other details of the malaria vector response to P. vivax infection.