Function of lipid binding proteins of parasitic helminths: still a long road

Lombardo, Jose F; Pórfido, Jorge Luis; Sisti, Martín Sebastián; Giorello, Antonella; Rodrı́guez, Santiago; Córsico, Betina; Franchini, Gisela Raquel

doi:10.1007/s00436-022-07463-1

Cited by 7 publications

(2 citation statements)

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“…In particular, Platyhelminthes are unable to synthesise fatty acids de novo [ 64 ], thus relying on the host’s lipid reservoir to ensure their survival. Several fatty acid-binding proteins (FABPs) have been identified in trematode species, such as Schistosoma spp., Fasciola spp and, most recently, in the diplozoid monogenean Eudiplozoon nipponicum [ 65 , 66 ]. Although FABPs have been described to play a role in fatty acid uptake by Fasciola hepatica from host blood and in immunomodulation, their function in monogeneans remains unknown [ 65 ].…”

Section: Discussionmentioning

confidence: 99%

“…and Fasciola spp. and the diplozoid monogenean E. nipponicum , it has been suggested that the host’s incorporated lipids may play important roles in maintaining different cellular structures after their distribution and storage in the parasite’s body or they may also be found in excretion/secretion products, which are involved in the modulation of the host’s immune system [ 66 , 67 ]. The human trematode Schistosoma mansoni has been described to bind part of the host’s LDL to their surface, which might be an immune evasion strategy, in addition to ingesting LDL, breaking it down and distributing lipids throughout the worm [ 72 ].…”

Section: Discussionmentioning

confidence: 99%

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A bloody interaction: plasma proteomics reveals gilthead sea bream (Sparus aurata) impairment caused by Sparicotyle chrysophrii

et al. 2022

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Background Sparicotylosis is an enzootic parasitic disease that is well established across the Mediterranean Sea. It is caused by the polyopisthocotylean monogenean Sparicotyle chrysophrii and affects the gills of gilthead sea bream (GSB; Sparus aurata). Current disease management, mitigation and treatment strategies are limited against sparicotylosis. To successfully develop more efficient therapeutic strategies against this disease, understanding which molecular mechanisms and metabolic pathways are altered in the host is critical. This study aims to elucidate how S. chrysophrii infection modulates the plasma proteome of GSB and to identify the main altered biological processes involved. Methods Experimental infections were conducted in a recirculating aquaculture system (RAS) in which naïve recipient GSB ([R]; 70 g; n = 50) were exposed to effluent water from S. chrysophrii-infected GSB (98 g; n = 50). An additional tank containing unexposed naïve fish (control [C]; 70 g; n = 50) was maintained in parallel, but with the open water flow disconnected from the RAS. Haematological and infection parameters from sampled C and R fish were recorded for 10 weeks. Plasma samples from R fish were categorised into three different groups according to their infection intensity, which was based on the number of worms fish−1: low (L: 1–50), medium (51–100) and high (H: > 100). Five plasma samples from each category and five C samples were selected and subjected to a SWATH-MS proteome analysis. Additional assays on haemoglobin, cholesterol and the lytic activity of the alternative complement pathway were performed to validate the proteome analysis findings. Results The discriminant analysis of plasma protein abundance revealed a clear separation into three groups (H, M/L and C). A pathway analysis was performed with the differentially quantified proteins, indicating that the parasitic infection mainly affected pathways related to haemostasis, the immune system and lipid metabolism and transport. Twenty-two proteins were significantly correlated with infection intensity, highlighting the importance of apolipoproteins, globins and complement component 3. Validation assays of blood and plasma (haemoglobin, cholesterol and lytic activity of alternative complement pathway) confirmed these correlations. Conclusions Sparicotylosis profoundly alters the haemostasis, the innate immune system and the lipid metabolism and transport in GSB. This study gives a crucial global overview of the pathogenesis of sparicotylosis and highlights new targets for further research. Graphical Abstract

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