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- BookBen Adler, editor.Summary: Spirochetes comprise a fascinating group of bacteria. Although diverse in terms of their habitat, ecology and infectivity for vertebrate and non-vertebrate hosts, they are often considered together because of their similar cellular morphologies. This volume brings together an international group of experts to provide essential insights into spirochete biology, with an emphasis on recent advances made possible by the availability of genome sequences. As such, it offers a valuable resource for microbiologists and other scientists with an interest in spirochete biology.
Contents:
The Treponema pallidum Outer Membrane
Gene regulation, two component regulatory systems, and adaptive responses in Treponema denticola
Physiologic and Genetic Factors Influencing the Zoonotic Cycle of Borrelia burgdorferi
Regulation of gene and protein expression in the Lyme disease spirochete
Genetic manipulation of Borrelia spp.
Toolbox of molecular techniques for studying Leptospira spp.
Interaction of Leptospira with the innate immune system
Leptospiral genomics and pathogenesis
Complement immune evasion by spirochetes
Spirochetal lipoproteins in pathogenesis and immunity
Colonic spirochetes: what has genomics taught us? .Access via Current topics in microbiology and immunology ; 2018; 415.LocationVersionCall NumberItems - ArticleKawanishi H.Am J Dig Dis. 1978 Feb;23(2):97-109.Using an in vitro system of antibody-dependent cellular cytotoxicity (ADCC), the killing effect of chronic liver disease sera on target Chang cells, mediated by effector nonimmune lymphocytes (NLy), was studied. NLy destroyed Chang cells in monolayers pretreated with sera of patients with chronic active liver disease (CALD). Sera from these patients with CALD, after receiving steroid therapy, demonstrated a significant decrease of the cytotoxic action of NLy. The target cells treated with sera of normal subjects or patients with chronic persistent hepatitis were only minimally affected. Morphological observations of the cytotoxic action in a CALD serum-treated group showed intimate contact between NLy and the target cells in the areas of the plaques, where large numbers of the target Chang cells were injured and were closely associated with effector NLy. The Chang cells developed cytoplasmic swelling. The surface became ruffled, and intracytoplasmic organelles displayed vesicular degeneration. Thereafter, cell rupture, and fragmentation occurred. The sera in patients with CALD appear to possess a membrane reactive factor, presumably antibody, against the surface membrane of Chang cells. This immunological mode of reaction between the effectors and target cells (ADCC) may be important in the perpetuation and pathogenesis of hepatocyte death in CALD.