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Lipopolysaccharide deacylation by an endogenous lipase controls innate antibody responses to Gram-negative bacteria.

Abstract
T cell-independent type 1 agonists such as Gram-negative bacterial lipopolysaccharides can stimulate B lymphocytes to proliferate and produce antibodies by signaling through Toll-like receptors. This phenomenon is well established in vitro, yet polyclonal B cell responses after bacterial infection in vivo are often weak and short-lived. We show here that B cell proliferation and polyclonal antibody production in response to Gram-negative bacterial infection are modulated by acyloxyacyl hydrolase, a host enzyme that deacylates bacterial lipopolysaccharides. Deacylation of lipopolysaccharide occurred over several days, allowing lipopolysaccharide to act as an innate immune stimulant yet limiting the eventual amount of B cell proliferation and polyclonal antibody production. Control of lipopolysaccharide activation by acyloxyacyl hydrolase indicates that mammals can regulate immune responses to bacterial infection by chemical modification of a Toll-like receptor agonist.
AuthorsMingfang Lu, Mei Zhang, Akira Takashima, Jerrold Weiss, Michael A Apicella, Xiang-Hong Li, Dorothy Yuan, Robert S Munford
JournalNature immunology (Nat Immunol) Vol. 6 Issue 10 Pg. 989-94 (Oct 2005) ISSN: 1529-2908 [Print] United States
PMID16155573 (Publication Type: Comparative Study, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Antibodies, Bacterial
  • Lipopolysaccharides
  • Carboxylic Ester Hydrolases
  • acyloxyacyl hydrolase
Topics
  • Acetylation
  • Animals
  • Antibodies, Bacterial (analysis)
  • B-Lymphocytes (immunology)
  • Carboxylic Ester Hydrolases (deficiency, genetics, metabolism)
  • Cell Division
  • Immunity, Innate
  • Immunization
  • Lipopolysaccharides (immunology, metabolism)
  • Lymph Nodes (immunology)
  • Mice
  • Neisseria meningitidis (immunology)
  • Spleen (immunology)

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