2 research outputs found

    How Strongly Do Oysters Stick?

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    Biological adhesives are a type of interfacial material that has incredible potential to generate new biomimetic compounds that can replace current strong, but toxic, adhesives. Therefore, a study of the chemical composition and mechanical properties of those bio-adhesives is necessary. However, in the case of oysters, despite known chemical characterization of the adult’s adhesive, there are almost no studies on its mechanical properties. Furthermore, there is no available information on the adhesive properties of spat (oysters in their larvae state). Herein, we present the first mechanical characterization of the spat adhesive, measuring its adhesion strength by hydrodynamic determination using a water jet. This study suggests that the adhesion strength of spat could be as high as 70 Pascals, but is highly dependent on experimental conditions. For instance, it was found that the adhesion strength increases on hydrophobic substrates with low surface energy, and that is also dependent on the environmental conditions, like the moisture level. Nevertheless, no relationship between the area of the larvae and its adhesion strength was found. Therefore, it can be proposed that a possible strong hydrophobic interaction adhesive-surface, or an enhancement of the adhesive production over low energy substrates is required for adhesive bonding. This would direct future studies on the search of the adhesion mechanism of this species and increase the biological knowledge about oyster larvae

    A Toxoplasma gondii lipoxygenase-like enzyme is necessary for virulence and changes localization associated with the host immune response

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    ABSTRACT While the asexual cycle of Toxoplasma gondii can occur in any warm-blooded animal, the sexual cycle is restricted to the feline intestine. We previously determined that because cats lack delta-6-desaturase activity in their intestines, they build up excess linoleic acid, which signals T. gondii to undergo sexual development. We hypothesized that T. gondii oxygenates linoleic acid to signal sexual development, so we examined the T. gondii genome for lipoxygenases-like enzymes (TgLOXL) enzymes. We identified seven TgLOXLs that were at least 100-fold more abundant in the cat intestinal versus the tissue culture tachyzoite stage. Parasites deleted in TgLOXL1 (TgΔLOXL1) had no significant growth differences in tissue culture fibroblast cells. Because the sexual development assay begins with brain cysts, we infected mice with TgΔLOXL1 and were surprised to find that TgΔLOXL1 had reduced virulence. The TgΔLOXL1 parasitemia was reduced by 3 d post-infection and largely cleared by 7 d post-infection. At 3 d post-infection, the cytokines interferon gamma (IFN-γ), IL-6, MCP-1, and TNF-α were significantly reduced in TgΔLOXL1-infected mice, which prompted us to examine TgΔLOXL1 in IFN-γ KO mice. We found that IFN-γ KO mice infected with TgΔLOXL1 succumbed to acute infection with the same kinetics as the parental and complemented strains, suggesting that TgLOXL1 plays a role in the IFN-γ signaling cascade. In tissue culture fibroblasts, TgLOXL1 was localized within the parasite, but in leukocytes from infected mice and activated macrophages, TgLOXL1 was localized within the host cytoplasm. These results suggest that TgLOXL1 changes localization in response to host immune activation. IMPORTANCE Lipoxygenases (LOXs) are enzymes that catalyze the deoxygenation of polyunsaturated fatty acids such as linoleic and arachidonic acid. These modifications create signaling molecules that are best characterized for modulating the immune response. Deletion of the first lipoxygenase-like enzyme characterized for Toxoplasma gondii (TgLOXL1) generated a less virulent strain, and infected mice showed a decreased immune response. This virulence defect was dependent on the mouse cytokine interferon gamma IFNγ. TgLOXL1 changes location from inside the parasite in tissue culture conditions to vesicular structures within the host immune cells during mouse infection. These results suggest that TgLOXL1 plays a role in the modification of the host immune response in mice
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