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. 2008;32(9):1050-62.
doi: 10.1016/j.dci.2008.02.003. Epub 2008 Mar 10.

Cuticular surface lipids are responsible for disguise properties of an entomoparasite against host cellular responses

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Cuticular surface lipids are responsible for disguise properties of an entomoparasite against host cellular responses

Maristella Mastore et al. Dev Comp Immunol. 2008.

Abstract

Entomopathogenic nematodes are widely used as alternatives to chemicals for the biological control of insects. These endoparasites are symbiotically associated with bacteria that are lethal for the host; however, parasites need to overcome the host immune defences to complete a successful life cycle. The processes parasites employ to escape or depress host immunity are targeted at deceiving non-self recognition as well as inactivating defence reactions. The purpose of this paper is to investigate the interactions between the entomopathogenic nematode Steinernema feltiae and the lepidopteran Galleria mellonella, focusing on the role of the parasite's body-surface compounds in the immunoevasion of host cell-mediated responses. To evaluate host self/non-self discrimination and encapsulation efficiency, we carried out a series of interaction assays between cultured host hemocytes and parasites or isolated cuticles. The data obtained suggest that the parasite cuticular lipids (PCLs) are able to bind a variety of host hemolymph molecules; PCLs attract host proteins from the hemolymph creating a coat around the parasite, thus, enabling Steinernema to disguise itself against hemocytes recognition. The role of parasite lipids in the disguise process was also investigated by simulating the nematode body surface with agarose microbeads covered with purified cuticular components; when the beads were coated with cuticular lipids, host hemocytes were not able to recognize and encapsulate. Results suggest that by means of attracting host hemolymph components onto its cuticular surface, S. feltiae prevents hemocytes attachment to its cuticle and inhibits melanization by depleting hemolymph components.

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