Lectin-Based Food Poisoning: A New Mechanism of Protein Toxicity

BACKGROUND: Ingestion of the lectins present in certain improperly cooked vegetables can result in acute GI tract distress, but the mechanism of toxicity is unknown. In vivo, gut epithelial cells are constantly exposed to mechanical and other stresses and consequently individual cells frequently experience plasma membrane disruptions. Repair of these cell surface disruptions allows the wounded cell to survive: failure results in necrotic cell death. Plasma membrane repair is mediated, in part, by an exocytotic event that adds a patch of internal membrane to the defect site. Lectins are known to inhibit exocytosis. We therefore tested the novel hypothesis that lectin toxicity is due to an inhibitory effect on plasma membrane repair. METHODS AND FINDINGS: Repair of plasma membrane disruptions and exocytosis of mucus was assessed after treatment of cultured cell models and excised segments of the GI tract with lectins. Plasma membrane disruptions were produced by focal irradiation of individual cells, using a microscope-based laser, or by mechanical abrasion of multiple cells, using a syringe needle. Repair was then assessed by monitoring the cytosolic penetration of dyes incapable of crossing the intact plasma membrane. We found that cell surface-bound lectins potently inhibited plasma membrane repair, and the exocytosis of mucus that normally accompanies the repair response. CONCLUSIONS: Lectins potently inhibit plasma membrane repair, and hence are toxic to wounded cells. This represents a novel form of protein-based toxicity, one that, we propose, is the basis of plant lectin food poisoning

Influence of the distribution and infection rates of psyllids on the vectoring ability of European stone fruit yellows in Switzerland

International audienceEuropean stone fruit yellows (ESFY) is caused by the phytoplasma ‘Candidatus Phytoplasma prunorum’, which is transmitted from plant to plant by insects of the genus Cacopsylla. Better knowledge of vector distribution in the orchards and on wild host plants is crucial for controlling the disease and preventing its spread. Cacopsylla pruni is known as the vector of ESFY. Recently, a second psyllid, Cacopsylla pinihiemata, has been identified as a vector; however, its vectoring capacity for ESFY phytoplasma is still unknown. The objective of this study was to map the distribution of psyllids in Switzerland and to determine the percentage of infested adults. The occurrence of psyllid species was monitored by sweeping techniques, and the percentage of infested adults was analyzed by nested PCR. Psyllid monitoring revealed that C. pruni is present in every Swiss region, with a similar population density in the different locations. In contrast, C. pinihiemata was only captured in Valais (southwest), the main apricot production area. This is probably due to the presence of specific conifers, which are the overwintering hosts for C. pinihiemata. Infested psyllid adults were found in half of the monitored regions. The percentage varied between 1.3 and 18.2% and was not higher in the apricot production area. Surprisingly, in 2013, ESFY infestation was only found in C. pruni and not in C. pinihiemata. However, in 2012, C. pinihiemata was also infested by ‘Ca. P. prunorum’. The capacity of the two psyllids in ESFY vectoring, their importance in ESFY epidemiology and the consequences on ESFY control strategies are discussed

Co-acquired nanovirus and geminivirus exhibit a contrasted localization within their common aphid vector

Single-stranded DNA (ssDNA) plant viruses belong to the families Geminiviridae and Nanoviridae. They are transmitted by Hemipteran insects in a circulative, mostly non-propagative, manner. While geminiviruses are transmitted by leafhoppers, treehoppers, whiteflies and aphids, nanoviruses are transmitted exclusively by aphids. Circulative transmission involves complex virus-vector interactions in which epithelial cells have to be crossed and defense mechanisms counteracted. Vector taxa are considered a relevant taxonomic criterion for virus classification, indicating that viruses can evolve specific interactions with their vectors. Thus, we predicted that, although nanoviruses and geminiviruses represent related viral families, they have evolved distinct interactions with their vector. This prediction is also supported by the non-structural Nuclear Shuttle Protein (NSP) that is involved in vector transmission in nanoviruses but has no similar function in geminiviruses. Thanks to the recent discovery of aphid-transmitted geminiviruses, this prediction could be tested for the geminivirus alfalfa leaf curl virus (ALCV) and the nanovirus faba bean necrotic stunt virus (FBNSV) in their common vector, Aphis craccivora. Estimations of viral load in midgut and head of aphids, precise localization of viral DNA in cells of insect vectors and host plants, and virus transmission tests revealed that the pathway of the two viruses across the body of their common vector differs both quantitatively and qualitatively