Nature Immunology
6, 989 - 994 (2005)
Published online: 11 September 2005; | doi:10.1038/ni1246
Lipopolysaccharide deacylation by an endogenous lipase controls innate antibody responses to Gram-negative bacteriaMingfang Lu1, Mei Zhang1, Akira Takashima2, Jerrold Weiss3, Michael A Apicella3, Xiang-Hong Li1, Dorothy Yuan4
& Robert S Munford1, 51
Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. 2
Department of Dermatology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. 3
Department of Internal Medicine and Department of Microbiology, University of Iowa, Iowa City, Iowa 52242, USA. 4
Department of Pathology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. 5
Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Correspondence should be addressed to Robert S Munford robert.munford@utsouthwestern.edu 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.
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