Biomphalaria glabrata infected with Angiostrongylus cantonensis: Proteomic changes in the snail host.

Abstract:

:Angiostrongylus cantonensis is the main cause of human eosinophilic meningitis. Humans are accidental hosts, becoming infected due to ingestion of raw intermediate (snails and slugs) or paratenic hosts. Once ingested, the larvae migrate towards the brain where they die, causing the disease. To develop better mollusk control strategies, it is important to first understand what happens in the snail during infection, therefore our purpose was to characterize proteomic, metabolic and immunologic changes in Biomphalaria glabrata 24 h after infection with A. cantonensis. For this purpose, proteins were extracted from infected and uninfected snails and analyzed through mass spectrometry. Hemolymph was also collected, the number of hemocytes was counted and urea, nitric oxide, calcium, glycogen levels as well as alanine and aspartate aminotransferases activities were assessed. The cephalopodal region and gonad-digestive gland complex were dissected and their glycogen content was measured. After infection with A. cantonensis, we observed an increase of hemocytes and granulocytes as well as an increase in hemoglobin type 2 proteins. Temptin-like protein was also found up-regulated in infected snails. Several proteins with structural function (such as myosin heavy chain - striated muscle - like and protein LOC106059779 with ADAM/reprosolin domain) were also differentially expressed, suggesting loss/damage of internal tissues. Increase in phosphoglycerate mutase indicates an increase in glycolysis, possible to compensate the increase in energetic needs. Consequently, there is a decrease in glycogen reserves, particularly in the gonad - digestive gland complex.

journal_name

Acta Trop

journal_title

Acta tropica

authors

Mendes TMF,Carrilho E,Galinaro CA,Cabral FJ,Allegretti SM

doi

10.1016/j.actatropica.2020.105684

subject

Has Abstract

pub_date

2020-12-01 00:00:00

pages

105684

eissn

0001-706X

issn

1873-6254

pii

S0001-706X(20)30157-1

journal_volume

212

pub_type

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