Induction of Proinflammatory Responses in Human Monocytes by Particulate and Soluble Forms of Lipopolysaccharide

Leeson, Michael C.; Morrison, David C.

doi:10.1097/00024382-199410000-00001

Cited by 36 publications

(17 citation statements)

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“…Indeed, for LPS it was found that soluble LPS is a more potent stimulus for TNF production than particulate, bacterium-bound LPS or LPS coated onto latex-beads (Leeson and Morrison 1994). There must thus be a difference in the ability of LTA and LPS to evoke receptor clustering.…”

Section: Article In Pressmentioning

confidence: 99%

Presentation of lipoteichoic acid potentiates its inflammatory activity

Deininger¹,

Traub²,

Aichele³

et al. 2008

Immunobiology

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Lipoteichoic acid (LTA) is a major immunostimulatory molecule in the cell wall of Gram-positive bacteria. Adhesion of LTA to a polystyrene surface drastically increased its immunostimulatory potency in human whole blood in comparison to soluble LTA, although only 1% of the LTA had bound, as determined using rhodamine-labelled LTA. The release of the proinflammatory cytokines IL-1beta, TNF and IL-6 and the chemokines IL-8 and G-CSF was increased 2- to 10-fold, but IL-10 release was unaltered. This presentation effect was not shared by lipopolysaccharide (LPS) or other toll-like receptor 2 agonists and was less pronounced in polypropylene vessels. LTA did not induce cytokine release in silicone-coated borosilicate vessels, but covalent coupling of LTA to polystyrene beads restored cytokine induction in these vessels, indicating that presentation of LTA on a surface is in fact essential for its immunostimulatory potency. This novel aspect of presentation as a factor in the recognition of LTA may reflect the physiological situation in the bacterial cell wall, where LTA is anchored in the bacterial membrane and projects through the peptidoglycan. In practical terms, contamination of medical devices with components of Gram-positive bacteria may pose an underestimated inflammatory risk.

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Section: Article In Pressmentioning

confidence: 99%

Presentation of lipoteichoic acid potentiates its inflammatory activity

Deininger¹,

Traub²,

Aichele³

et al. 2008

Immunobiology

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“…Endotoxin may be liberated spontaneously during multiplication of microorganisms, however, its release has been shown to be precipitated and intensified by the antibiotic-induced disintegration of bacteria. Compared to cell-bound endotoxin, soluble endotoxin released from bacteria as a result of antibiotic exposure may have an up to 50-fold increase in biological activity [46]. In the past two decades in vitro studies have also shown that exposure to antibiotics boosts endotoxin-release from Gram-negative microorganisms [47,48,49].…”

Section: Antibiotic-induced Release Of Bacterial Cell Wall Componentsmentioning

confidence: 99%

Clinical implications of antibiotic-induced endotoxin release in septic shock

et al. 2002

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Antibiotic-induced release of bacterial cell wall components can have immediate adverse effects for the patient. This article reviews the data on endotoxin release after initiation of antibiotic therapy and its role in the pathogenesis of sepsis and septic shock. Antibiotics differ in their potential to liberate endotoxins from bacterial cell walls. When used for treatment of systemic Gram-negative infection, some classes of beta-lactam antibiotics lead to markedly increased levels of free endotoxins while treatment with carbapenems and aminoglycosides produces relatively low amounts of endotoxins. Antibiotics that induce the formation of long, aberrant bacterial cells before effectively killing the microorganisms show the highest degree of endotoxin liberation. There is increasing evidence from animal models and clinical studies of sepsis that the antibiotic-mediated release of biologically active cell wall components derived from Gram-positive, Gram-negative or fungal organisms is associated with a rapid clinical deterioration.

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“…We have observed a very similar TNF-␣ response in RAW 264.7 cells (Table I) treated with equivalent concentrations of either nonconjugated or gold-conjugated ReLPS (5-or 30-nm gold conjugates did not show any difference in activity). Therefore, we used colloidal gold as the label, because in previous studies it was shown that picogram concentrations of LPS coated on latex beads generated less than 50% of soluble LPS induction of procoagulant activity in cultured monocytes (32). The effect was probably attributable to the relatively large size of latex beads (0.114 m) used in that study.…”

Section: Characterization Of Relps-and Rsdpla-gold Conjugatesmentioning

confidence: 99%

Diphosphoryl Lipid A from Rhodobacter sphaeroides Blocks the Binding and Internalization of Lipopolysaccharide in RAW 264.7 Cells

Kutuzova

Albrecht

Erickson

et al. 2001

The Journal of Immunology

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Diphosphoryl lipid A derived from the nontoxic LPS of Rhodobacter sphaeroides (RsDPLA) has been shown to be a powerful LPS antagonist in both human and murine cell lines. In addition, RsDPLA also can protect mice against the lethal effects of toxic LPS. In this study, we complexed both the deep rough LPS from Escherichia coli D31 m4 (ReLPS) and RsDPLA with 5- and 30-nm colloidal gold and compared their binding to the RAW 264.7 cell line by electron microscopy. Both ReLPS and RsDPLA bound to the cells with the following observations. First, binding studies revealed that pretreatment with RsDPLA completely blocked the binding and thus internalization of ReLPS-gold conjugates to these cells at both 37°C and 4°C. Second, ReLPS was internalized via micropinocytosis (noncoated plasma membrane invaginations) involving formation of caveolae-like structures and leading to the formation of micropinocytotic vesicles, macropinocytosis (or phagocytosis), formation of clathrin-coated pits (receptor mediated), and penetration through plasma membrane into cytoplasm. Third, in contrast, RsDPLA was internalized predominantly via macropinocytosis. These studies show for the first time that RsDPLA blocks the binding and thus internalization of LPS as observed by scanning and transmission electron microscopy.

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Induction of Proinflammatory Responses in Human Monocytes by Particulate and Soluble Forms of Lipopolysaccharide

Cited by 36 publications

References 0 publications

Presentation of lipoteichoic acid potentiates its inflammatory activity

Presentation of lipoteichoic acid potentiates its inflammatory activity

Clinical implications of antibiotic-induced endotoxin release in septic shock

Diphosphoryl Lipid A from Rhodobacter sphaeroides Blocks the Binding and Internalization of Lipopolysaccharide in RAW 264.7 Cells

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