Publications by authors named "Lisa Barroso"

Amebiasis in the murine model can be prevented by vaccination with the Gal/GalNAc lectin through a T cell-dependent mechanism. In this work we further decipher the mechanism of this protection. Mice vaccinated with the recombinant "LecA" fragment of the Gal/GalNAc lectin with alum were capable of transferring protection to naïve recipients by both CD4+ T cells and surprisingly CD8+ T cells.

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Article Synopsis
  • The study confirms that a vaccine using the Entamoeba histolytica Gal/GalNAc lectin protects mice from intestinal amebiasis through T cell-mediated immunity, not antibodies.
  • Vaccination resulted in the production of important cytokines like IFN-gamma and IL-12, indicating a robust T cell response.
  • The research shows that subcutaneous vaccination with a specific adjuvant achieved the highest efficacy (79%), while different routes and adjuvants provided varying levels of protection, all highlighting the crucial role of IFN-gamma in vaccine effectiveness.
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Prevention of intestinal infection by Entamoeba histolytica would block both invasive disease and parasite transmission. The amebic Gal/GalNAc lectin mediates parasite adherence to the colonic surface and fecal anti-lectin IgA is associated with protection from intestinal reinfection in children. We tested if vaccination with the E.

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RicinB, the non-toxic galactose/N-acetylgalactosamine-binding subunit of ricin, was fused to a model antigen, green fluorescent protein (GFP), and expressed in tobacco plants and hairy root cultures to test for utility in mucosal vaccine delivery/adjuvancy. The fusion protein retained both GFP fluorescence and galactose/galactosamine-binding activity. Intranasal immunization of mice with galactosamine-affinity purified ricinB:GFP recovered from tobacco root cultures triggered significant increases in GFP-specific serum IgGs.

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TxeR, a sigma factor that directs Clostridium difficile RNA polymerase to recognize the promoters of two major toxin genes, was shown to stimulate its own synthesis. Whether expressed in C. difficile, Clostridium perfringens, or Escherichia coli, TxeR stimulated transcription of fusions of the txeR promoter region to reporter genes.

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