The Journal of Immunology, Vol 144, Issue 4 1404-1410, Copyright © 1990 by American Association of Immunologists

ARTICLES

A comparison of the effects of intact and deacylated lipopolysaccharide on human polymorphonuclear leukocytes

AR Nogare and WC Yarbrough Jr
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.

Enzymatic deacylation of LPS markedly reduces its activity in the dermal Shwartzman reaction. Inasmuch as polymorphonuclear leukocytes (PMN) are involved in the genesis of tissue injury in Shwartzman reactions, we have investigated the effects of deacylated LPS (dLPS) on PMN. Compared to LPS, dLPS was ineffectual as a stimulus of both PMN adherence and release of secondary granule enzymes, and dLPS inhibited specific LPS-induced adherence. Neither LPS nor dLPS caused release of the primary granule enzymes, myeloperoxidase, and elastase. Unlike LPS, dLPS failed to prime PMN for superoxide release when a second stimulus (FMLP, 10(-6) M was given. The mechanism of the LPS induced increase in PMN adherence was investigated, and we found that LPS significantly increased the amount of the adhesive glycoprotein CD11b on the surface of the PMN. dLPS had no effect on CD11b expression. Our results suggest that enzymatic deacylation of LPS profoundly alters its ability to stimulate PMN and deacylation of LPS by inflammatory cells in vivo might be an important mechanism limiting the toxic effects of LPS.

This article has been cited by other articles:

				C. Alexander and E. Th. Rietschel Invited review: Bacterial lipopolysaccharides and innate immunity Innate Immunity, June 1, 2001; 7(3): 167 - 202. [Abstract] [PDF]

				B. Beutler and A. Poltorak The Sole Gateway to Endotoxin Response: How Lps Was Identified as Tlr4, and Its Role in Innate Immunity Drug Metab. Dispos., April 1, 2001; 29(4): 474 - 478. [Abstract] [Full Text]

				A. M. Soler-Rodriguez, H. Zhang, H. S. Lichenstein, N. Qureshi, D. W. Niesel, S. E. Crowe, J. W. Peterson, and G. R. Klimpel Neutrophil Activation by Bacterial Lipoprotein Versus Lipopolysaccharide: Differential Requirements for Serum and CD14 J. Immunol., March 1, 2000; 164(5): 2674 - 2683. [Abstract] [Full Text] [PDF]

				M.J. Cody, C.A. Salkowski, B.E. Henricson, G.R. Detore, R.S. Munford, and S.N. Vogel Effect of inflammatory and antiinflammatory stimuli on acyloxyacyl hydrolase gene expression and enzymatic activity in murine macrophages Innate Immunity, October 1, 1997; 4(5): 371 - 379. [Abstract] [PDF]

				R. L. Kitchens and R. S. Munford Enzymatically Deacylated Lipopolysaccharide (LPS) Can Antagonize LPS at Multiple Sites in the LPS Recognition Pathway J. Biol. Chem., April 28, 1995; 270(17): 9904 - 9910. [Abstract] [Full Text] [PDF]

				A. Poltorak, P. Ricciardi-Castagnoli, S. Citterio, and B. Beutler Physical contact between lipopolysaccharide and Toll-like receptor 4 revealed by genetic complementation PNAS, February 29, 2000; 97(5): 2163 - 2167. [Abstract] [Full Text] [PDF]