The Journal of Experimental Medicine
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Published 16 June 2003. doi:10.1084/jem.20030420
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© Rockefeller University Press, 0022-1007/2003/6/1745 $5.00
The Journal of Experimental Medicine, Volume 197, Number 12, 1745-1754

Stimulus-dependent Deacylation of Bacterial Lipopolysaccharide by Dendritic Cells

Mingfang Lu1, Mei Zhang1, Richard L. Kitchens1, Susan Fosmire1, Akira Takashima3 and Robert S. Munford1,2

1 Department of Internal Medicine, University of Texas, Southwestern Medical Center, Dallas, TX 75390
2 Department of Microbiology, University of Texas, Southwestern Medical Center, Dallas, TX 75390
3 Department of Dermatology, University of Texas, Southwestern Medical Center, Dallas, TX 75390

Address correspondence to R.S. Munford, Infectious Disease Division, Dept. of Internal Medicine, University of Texas, Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9113. Phone: 214-648-3480; Fax: 214-648-9478; E-mail: robert.munford{at}utsouthwestern.edu

We describe here a previously unrecognized property of dendritic cells (DCs), the ability to deacylate the lipid A moiety of gram-negative bacterial LPSs. Both immature DCs of the XS52 cell line and bone marrow–derived DCs produce acyloxyacyl hydrolase, an enzyme that detoxifies LPS by selectively removing the secondary acyl chains from lipid A. Acyloxyacyl hydrolase expression decreased when DCs were incubated with IL-4, IL-1ß, TNF{alpha}, and an agonistic CD40 antibody (maturation cocktail), and increased after treatment with LPS, CpG oligodeoxynucleotides, or a gram-positive bacterium (Micococcus luteus). Maturation cocktail treatment also diminished, whereas LPS treatment enhanced or maintained the cells' ability to kill Escherichia coli, deacylate LPS, and degrade bacterial protein. Enzymatic deacylation of LPS is an intrinsic, regulated mechanism by which DCs may modulate host responses to this potent bacterial agonist.

Key Words: lipopolysaccharide • dendritic cell • acyoxyacyl hydrolase • gram-negative bacteria • deacylation


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