Browsing by MeSH term "Host-Parasite Interactions"
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Publication Differentiation and gene flow among European populations of Leishmania infantum MON-1(Public Library of Science (PLOS), 2008-07-09) Kuhls, Katrin; Chicharro, Carmen; Cañavate, Carmen; Cortes, Sofia; Campino, Lenea; Haralambous, Christos; Soteriadou, Ketty; Pratlong, Francine; Dedet, Jean-Pierre; Mauricio, Isabel; Miles, Michael; Schaar, Matthias; Ochsenreither, Sebastian; Radtke, Oliver A; Schönian, Gabriele; Unión EuropeaBACKGROUND: Leishmania infantum is the causative agent of visceral and cutaneous leishmaniasis in the Mediterranean region, South America, and China. MON-1 L. infantum is the predominating zymodeme in all endemic regions, both in humans and dogs, the reservoir host. In order to answer important epidemiological questions it is essential to discriminate strains of MON-1. METHODOLOGY/PRINCIPAL FINDINGS: We have used a set of 14 microsatellite markers to analyse 141 strains of L. infantum mainly from Spain, Portugal, and Greece of which 107 strains were typed by MLEE as MON-1. The highly variable microsatellites have the potential to discriminate MON-1 strains from other L. infantum zymodemes and even within MON-1 strains. Model- and distance-based analysis detected a considerable amount of structure within European L. infantum. Two major monophyletic groups-MON-1 and non-MON-1-could be distinguished, with non-MON-1 being more polymorphic. Strains of MON-98, 77, and 108 were always part of the MON-1 group. Among MON-1, three geographically determined and genetically differentiated populations could be identified: (1) Greece; (2) Spain islands-Majorca/Ibiza; (3) mainland Portugal/Spain. All four populations showed a predominantly clonal structure; however, there are indications of occasional recombination events and gene flow even between MON-1 and non-MON-1. Sand fly vectors seem to play an important role in sustaining genetic diversity. No correlation was observed between Leishmania genotypes, host specificity, and clinical manifestation. In the case of relapse/re-infection, only re-infections by a strain with a different MLMT profile can be unequivocally identified, since not all strains have individual MLMT profiles. CONCLUSION: In the present study for the first time several key epidemiological questions could be addressed for the MON-1 zymodeme, because of the high discriminatory power of microsatellite markers, thus creating a basis for further epidemiological investigations.Publication Hookworms Evade Host Immunity by Secreting a Deoxyribonuclease to Degrade Neutrophil Extracellular Traps.(Cell Press, 2020) Bouchery, Tiffany; Moyat, Mati; Sotillo, Javier; Silverstein, Solomon; Volpe, Beatrice; Coakley, Gillian; Tsourouktsoglou, Theodora-Dorita; Becker, Luke; Shah, Kathleen; Kulagin, Manuel; Guiet, Romain; Camberis, Mali; Schmidt, Alfonso; Seitz, Arne; Giacomin, Paul; Le Gros, Graham; Papayannopoulos, Venizelos; Loukas, Alex; Harris, Nicola L; Swiss National Science Foundation; National Health and Medical Research Council (Australia)Hookworms cause a major neglected tropical disease, occurring after larvae penetrate the host skin. Neutrophils are phagocytes that kill large pathogens by releasing neutrophil extracellular traps (NETs), but whether they target hookworms during skin infection is unknown. Using a murine hookworm, Nippostrongylus brasiliensis, we observed neutrophils being rapidly recruited and deploying NETs around skin-penetrating larvae. Neutrophils depletion or NET inhibition altered larvae behavior and enhanced the number of adult worms following murine infection. Nevertheless, larvae were able to mitigate the effect of NETs by secreting a deoxyribonuclease (Nb-DNase II) to degrade the DNA backbone. Critically, neutrophils were able to kill larvae in vitro, which was enhanced by neutralizing Nb-DNase II. Homologs of Nb-DNase II are present in other nematodes, including the human hookworm, Necator americanus, which also evaded NETs in vitro. These findings highlight the importance of neutrophils in hookworm infection and a potential conserved mechanism of immune evasion.Publication Plasma-derived extracellular vesicles from Plasmodium vivax patients signal spleen fibroblasts via NF-kB facilitating parasite cytoadherence.(Nature Publishing Group, 2020) Toda, Haruka; Diaz-Varela, Miriam; Segui-Barber, Joan; Roobsoong, Wanlapa; Baro, Barbara; Garcia-Silva, Susana; Galiano, Alicia; Gualdrón-López, Melisa; Almeida, Anne C G; Brito, Marcelo A M; de Melo, Gisely Cardoso; Aparici-Herraiz, Iris; Castro-Cavadía, Carlos; Monteiro, Wuelton Marcelo; Borràs, Eva; Sabidó, Eduard; Almeida, Igor C; Chojnacki, Jakub; Martinez-Picado, Javier; Calvo, Maria; Armengol, Pilar; Carmona-Fonseca, Jaime; Yasnot, Maria Fernanda; Lauzurica, Ricardo; Marcilla, Antonio; Galinski, Mary R; Lacerda, Marcus V G; Sattabongkot, Jetsumon; Fernandez-Becerra, Carmen; Del Portillo, Hernando A; Peinado Selgas, HectorPlasmodium vivax is the most widely distributed human malaria parasite. Previous studies have shown that circulating microparticles during P. vivax acute attacks are indirectly associated with severity. Extracellular vesicles (EVs) are therefore major components of circulating plasma holding insights into pathological processes. Here, we demonstrate that plasma-derived EVs from Plasmodium vivax patients (PvEVs) are preferentially uptaken by human spleen fibroblasts (hSFs) as compared to the uptake of EVs from healthy individuals. Moreover, this uptake induces specific upregulation of ICAM-1 associated with the translocation of NF-kB to the nucleus. After this uptake, P. vivax-infected reticulocytes obtained from patients show specific adhesion properties to hSFs, reversed by inhibiting NF-kB translocation to the nucleus. Together, these data provide physiological EV-based insights into the mechanisms of human malaria pathology and support the existence of P. vivax-adherent parasite subpopulations in the microvasculature of the human spleen.