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    Home > Active Ingredient News > Immunology News > PLoS patchogen: the key mechanism of how Salmonella typhi infects

    PLoS patchogen: the key mechanism of how Salmonella typhi infects

    • Last Update: 2020-02-26
    • Source: Internet
    • Author: User
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    February 27, 2020 / biourn / - a recent study found how Salmonella typhi recognizes the host's immune cells and releases toxins that damage the immune system The findings, published in PLoS patterns on February 21, provide a new direction for the development of typhoid treatment According to the Centers for Disease Control and prevention, Salmonella typhi infects 21 million people worldwide every year The disease is most common in areas with poor sanitation and unsafe water and food, including South Asia, especially Pakistan, India and Bangladesh (image source: www Pixabay Com) this study identified three subunits of typhoid toxin protein, one of which is the key to transfer toxin to host cells "Salmonella typhi is a life-threatening pathogen, but the underlying pathogenesis has not been well understood," said Zheng Min song, assistant professor of Microbiology and immunology at the school of veterinary medicine Tri Nguyen and sohyoung Lee, postdoctoral researchers at Song lab, were the first authors of the study "Here we show that a protein secreted by typhoid bacteria plays an important role in this pathogenesis," Song said The research focuses on a protein compound secreted by Salmonella typhi, which can help bacteria escape the host immune response The toxin consists of three protein subunits Two of these subunits are called "a" subunits; when they enter the host immune cells, they destroy the immune response The third "B" subunit recognizes and binds specific carbohydrate molecules on the surface of host immune cells, thus initiating the process of toxin entering cells The authors found that bacterial B-subunit recognized and attached to the surface of a trisaccharide molecule called N-acetylneuraminic acid B subunit can attach to unmodified trisaccharide, but it has higher affinity to the modified molecule Once attached, the toxin enters the cell Once in the immune cells, these two enzyme subunits will make the innate immune response of cells invalid These findings open the door to the development of drugs that block high affinity receptor molecules and inhibit toxins from entering target cells (BIOON Com) source of information: study finds key mechanism for how typed bacteria infections original source: tri Nguyen et al, the role of 9-O-acetylated glycan receiver locomotives in the typed toxin binding and introspection, PLoS patterns (2020) Doi: 10.1371/journal.ppat.1008336
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