Inhibition by lipid A-specific monoclonal antibodies of priming of human polymorphonuclear leucocytes by endotoxin

Cornelissen, J.J.; Kessel, Christoph; Brouwer, Eric; Kraaijeveld, C. A.; Verhoef, J.

doi:10.1099/00222615-34-4-233

Cited by 9 publications

(3 citation statements)

References 29 publications

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“…The generation of IgM MAbs against the O18 LPS and the K5 capsule has been described by Frasa et al (12). The two IgM MAbs directed against lipid A (MAbs 8-2C1 and 26-20) that we used have been described previously (4,5,10). An IgM MAb directed against Helicobacter spp.…”

Section: Methodsmentioning

confidence: 99%

Effect of imipenem on monoclonal antibody-mediated protection against Escherichia coli O18K5

Frasa¹,

Benaissa-Trouw²,

Tavares³

et al. 1996

Antimicrob Agents Chemother

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Flow cytometry revealed that the binding of immunoglobulin M monoclonal antibodies (MAbs) to Escherichia coli O18K5 was modulated by exposure of the bacteria to subinhibitory concentrations of imipenem. The binding of anti-K5 MAb was decreased, while the binding of anti-O18 MAb was increased. In addition, anti-lipid A MAbs bound only to imipenem-treated bacteria. The biological effect of MAb binding was investigated in BALB/c mice by determination of the levels of bacteremia, tumor necrosis factor (TNF) in serum and survival after intraperitoneal challenge with bacteria preincubated with MAb. Neither MAb alone (150 micrograms per animal) proved to be protective against untreated bacteria. Anti-lipid A MAb on its own, in contrast to anti-K5 and anti-O18 MAbs, was not protective against imipenem-treated bacteria. Only combinations which included anti-O18 MAb and anti-K5 MAb exerted in mice enhanced protection against smooth E. coli O18K5 as well as imipenem-treated E. coli O18K5. This was reflected by reduced TNF levels in serum and increased survival. The addition of anti-lipid A MAb to the combination of anti-K5 MAb and anti-O18 MAb reduced serum TNF levels in mice, but not significantly.

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Section: Methodsmentioning

confidence: 99%

Effect of imipenem on monoclonal antibody-mediated protection against Escherichia coli O18K5

Frasa¹,

Benaissa-Trouw²,

Tavares³

et al. 1996

Antimicrob Agents Chemother

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“…Human polyclonal antiserum produced against endotoxin core determinants has been shown to reduce mortality in clinical trials of patients experiencing Gram-negative bacteremia [96] and to reduce the incidence of septic shock in surgical patients at high risk [97]. Suggested mechanisms by which such protection may occur include inhibition of neutrophil priming by endotoxin [98], the enhancement of endotoxin binding clearance [99,100], and inhibition of TNF production [ 101,102]. This antiserum was produced by injecting volunteers with a mutant E. coli known as J5; this inducer strain yielded a relatively specific immune response to lipid A and other core components.…”

Section: Anti-endotoxin Antibodymentioning

confidence: 99%

Biological response modifiers and infectious diseases: Actual and potential therapeutic agents

Rusthoven

1994

International Journal of Antimicrobial Agents

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Biological response modifiers (BRMs) are agents which can modify the immune response to cancer or invasion of the organism by infectious agents. An explosive appearance of new BRMs has resulted from the development of recombinant gene technology and the availability of monoclonal antibodies. Colony-stimulating factors first became available for the prevention of neutropenia but may also have a role in the treatment of infections. Interleukin-1 is being tested as a modular of hematopoiesis and may be useful as a helper factor for T- and B-cell function. Immunoglobulins are being used against viral and bacterial infections while interferons can prevent viral upper respiratory infections and suppress or irradicate some viral hepatitides. Other BRMs which show promise include chemical agents and traditional herbal medicines.

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“…To study the influence of endotoxins on coagulation, pieces of peritoneum on the bottom of the wells were incubated for 4 hours with endotoxin (lipopolysaccharide of Salmonella minnesota Re595 [Re mutant], 100 ng/ml) 30 or in combination with polymixin B (50 /xg/ml, Sigma). All coagulation studies were started within 90 minutes after removal of these pieces from the abdomen.…”

Section: Surface Procoagulant Assaysmentioning

confidence: 99%

Thrombogenicity and procoagulant activity of human mesothelial cells.

Pronk¹,

Groot²,

Papendrecht³

et al. 1992

Arterioscler Thromb

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Cell seeding may decrease the thrombogenicity of implanted vascular grafts, but its application is hampered by the limited availability of autologous endothelial cells. We studied the interaction of alternate cells, human peritoneal mesothelial cells, with whole blood in a flow chamber. When titrated blood was perfused over mesothelial cells, platelet adhesion was seen on the intercellular matrix but not on the cells themselves. Pet-fusions with blood anticoagulated with low-molecular-weight heparin resulted in fibrin formation at the surface of mesothelial cells but not at the surface of human umbilical venous endothelial cells. At shear rates of 200 sec~' fibrin deposition on the mesothelial cell surface increased during the first 5 minutes to 5.7 ±1.06 fi% fibrin per square centimeter, whereafter these values stabilized. The procoagulant activity of cultured mesothelial cells was higher than that of peritoneal membrane studied ex vivo. However, cultured mesothelial cells incubated with polyclonal antibodies against tissue factor showed a significant decrease in procoagulant activity. We conclude that human peritoneal mesothelial cells may be used for cell seeding procedures, provided that their tissue factor expression can be controlled. 1 One of the causes for the inferior performance of prosthetic vascular grafts is thought to be their failure to establish a blood flowsupporting cellular surface.2 After implantation of a graft the lumen may be reduced by deposition of proteinaceous material and aggregated platelets. Consequently, the blood flow drops and may reach a critical level at which occlusion via thrombosis occurs. 3Previous workers have succeeded in seeding endothelial cells on vascular prostheses and have claimed reduced thrombogenicity of the implanted grafts. 4 -5 One of the major problems of endothelial cell seeding, however, is the limited availability of human endothelial cells. With current techniques, the luminal surface area of a donor vein that is needed to effectively seed a graft approximates half the surface area of that graft.67 In most cases it is then better to use the donor vein directly as a vascular conduit rather than as a source of endoFrom the Departments of Haematology (P.G. de G., J.J.S.) and Surgery (A.P., TJ.M.V. van V.), University Hospital Utrecht, and the Departments of Surgery (A.P., A.A.G.M.H. van P., P.L.) and Microbiology (H.A.V.),

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Inhibition by lipid A-specific monoclonal antibodies of priming of human polymorphonuclear leucocytes by endotoxin

Cited by 9 publications

References 29 publications

Effect of imipenem on monoclonal antibody-mediated protection against Escherichia coli O18K5

Effect of imipenem on monoclonal antibody-mediated protection against Escherichia coli O18K5

Biological response modifiers and infectious diseases: Actual and potential therapeutic agents

Thrombogenicity and procoagulant activity of human mesothelial cells.

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