Read e-book online Host-Microbe Interactions PDF


By Michael San Francisco and Brian San Francisco (Eds.)

ISBN-10: 0128093854

ISBN-13: 9780128093856

ISBN-10: 0128096179

ISBN-13: 9780128096178

Host-Microbe Interactions, the most recent quantity within the Progress in Molecular Biology sequence, offers a discussion board for the dialogue of recent discoveries, methods, and ideas in molecular biology. It comprises contributions from leaders of their respective fields, besides ample references. This quantity is devoted to the topic of host-microbe interactions.

  • Provides the most recent study on host-microbe interactions, together with new discoveries, techniques, and ideas
  • Contains contributions from top professionals on issues with regards to molecular biology
  • Informs and updates on all of the most modern advancements within the box

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Sample text

Hence, in-depth exploration of the mechanisms underlying pathogen–host interactions is 30 N. German et al. essential for understanding virulence-factor activation and defining therapeutic targets for potential antivirulence therapies. 14 At the same time, metal ions are known to cause cell toxicity by displacement of metal cofactors from various enzymes, rendering them inactive, as well as, through production of reactive oxygen species (ROS) (Fenton chemistry). The mechanism of the latter includes reaction of reduced form of transitions metals, such as, Fe, Cu, and Ni, with dissolved oxygen to produce superoxide.

ROS production leads to the damage of bacterial DNA, proteins, and lipids. Cu has been shown to induce damage of Fe–S clusters essential for bacterial survival and growth. As discussed earlier, Cu toxicity is employed by macrophages to eliminate pathogenic bacteria from the host organism. It was proposed that such mechanisms of bacterial killing originated in protozoa and evolved only later in eukaryotic phagocytes. 40 Therefore, 36 N. German et al. coevolution of bacteria and free-living unicellular eukaryote predators has predisposed bacteria to become pathogenic (opportunistically) in multicellular host organisms.

PcoE is controlled by CusRS, whereas, the expression of PcoABCD is primarily regulated by PcoRS. 46 This suggests that PcoE sequesters Cu in the periplasm, giving time for the remaining pco genes to be fully induced and the encoded proteins to function effectively. 2 Copper-Binding Siderophores It is well accepted that Cu-binding molecules in bacteria have evolved as defense tools, allowing the acquisition and/or neutralization of host-derived Cu. coli, is strongly linked to the expression of yersiniabactin (Ybt), a salicylate-based siderophore.

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Host-Microbe Interactions by Michael San Francisco and Brian San Francisco (Eds.)

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