Specific binding of lipopolysaccharides to mouse macrophages—I. Characteristics of the interaction and inefficiency of the polysaccharide region

Tahri-Jouti, Mohamed-Ali; Chaby, Richard

doi:10.1016/0161-5890(90)90084-d

Cited by 25 publications

(10 citation statements)

References 53 publications

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“…This hypothesis is supported by recent studies in mouse peritoneal macrophages in which binding of tritium-labelled LPS was strongly blocked by dexamethasone, over the same concentration range as used in our study (Tahri-Jouti & Chaby, 1990). The fact that dexamethasone could not reverse a vasodilatation induced by LPS suggests that LPS may avidly bind -to its recognition sites on the endothelium and may not be easily displaced.…”

Section: Discussionsupporting

confidence: 90%

Bacterial endotoxin rapidly stimulates prolonged endothelium‐dependent vasodilatation in the rat isolated perfused heart

Baydoun

Foale

Mann

1993

British J Pharmacology

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1 The effects of bacterial lipopolysaccharide (Escherichia coli 011 1-B4; LPS) on coronary vascular tone were examined in the isolated perfused heart of the rat. The role of nitric oxide and/or prostaglandin products of the cyclo-oxygenase pathway in mediating the actions of LPS were also investigated. 2 Coronary vascular tone was raised and maintained by a continuous perfusion of the thromboxanemimetic U46619 (5nM). LPS perfusion (0.1-100itgml-') caused a concentration-dependent fall in coronary tone without any significant change in the force of cardiac contractility.3 At 5 lggml', LPS reduced perfusion pressure by 38±9mmHg. This effect was rapid in onset, maximal within the first 5 min and sustained for 90 + 10 min (n = 6). 4 The vasodilatation induced by LPS was dependent on the presence of an intact endothelium and abolished following endothelial damage caused by air embolism.5 NW-nitro-L-arginine methylester (L-NAME; 50 gM) or N0-nitro-L-arginine (L-NOARG; 50 tM) blocked the vasodilatation induced by LPS (5 jLg ml--). The inhibition caused by these arginine analogues was partially reversed by 1 mM L-but not D-arginine. 6 The vasodilator action of LPS was also completely blocked by the glucocorticoid, dexamethasone (10 jiM) but unaffected by indomethacin (10 jiM).7 These results suggest that LPS evokes rapid release of nitric oxide (NO) in the microvasculature of the rat isolated heart presumably via activation of the constitutive L-arginine-NO pathway in the endothelium. Furthermore, the lack of effect of indomethacin suggests that prostaglandins released via the cyclo-oxygenase pathway are not involved in mediating this action of LPS.

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Section: Discussionsupporting

confidence: 90%

Bacterial endotoxin rapidly stimulates prolonged endothelium‐dependent vasodilatation in the rat isolated perfused heart

Baydoun

Foale

Mann

1993

British J Pharmacology

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“…An activating role of albumin on endotoxin activity in vitro and in vivo has been previously shown (23,43,46). Complexes of albumin with isolated lipid A or intact LPS are bioactive, especially when presented in disaggregated form (27,42,(47)(48)(49)(50). Our findings also show a striking parallel between albumin-dependent disaggregation of endotoxin and endotoxin-dependent cell activation (Figs.…”

Section: Albumin Is Needed As a Cofactor For Los:scd14 Complex-supporting

confidence: 60%

An Essential Role for Albumin in the Interaction of Endotoxin with Lipopolysaccharide-binding Protein and sCD14 and Resultant Cell Activation

Gioannini

Zhang

Teghanemt

et al. 2002

Journal of Biological Chemistry

118

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Experiments utilizing endotoxin aggregates, lipooligosaccharides (LOS) isolated from metabolically labeledNeisseria meningitidis serotype group B, demonstrate that albumin is an essential component of lipopolysaccharide binding protein-(LBP) and sCD14-dependent 1) disaggregation of LOS and 2) LOS activation of human umbilical vein endothelial cells (HUVEC). Aggregates of LOS (LOS agg ) with an apparent M r > 2 ؋ 10 7 were isolated by gel sieving on Sephacryl HR S500 in buffered balanced salts solution plus albumin. Incubation of LOS agg with LBP and sCD14 promoted LOS agg disaggregation in an albumin-dependent fashion to complexes that contain LOS and sCD14, but no LBP, with an apparent M r ϳ 60,000 (LOS:sCD14) as determined by Sephacryl S200 chromatography. Isolation by gel filtration of LOS agg :protein aggregates formed by the interaction of LOS agg with either LBP or sCD14 alone revealed that the sequence of LOSprotein interactions as well as the step(s) at which albumin is necessary for the production of bioactive LOS: sCD14 were specific. Efficient generation of LOS:sCD14 required 1) interaction of LOS agg with LBP before interaction with CD14 and 2) the presence of albumin during the interaction of LBP with LOS agg . Activation of HUVEC by LOS agg , as measured by IL-8 production, required both LBP and sCD14 and was thirty times more potent in the presence of albumin. In contrast, LOS:sCD14 did not require additional LBP, sCD14, or albumin to activate HUVEC but depended on the presence of albumin for optimal solubility/stability once formed. The albumin effect is apparently specific, because neither ovalbumin nor gelatin substituted for albumin in facilitating LBP:sCD14-dependent disaggregation of LOS agg or activation of endothelial cells. These results indicate that albumin is an essential facilitator of LBP/sCD14-induced LOS disaggregation that is required for activation of endothelial cells by LOS agg .

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“…Furthermore, this effect was observed with concentrations of dexamethasone well below the standard pharmacological concentrations routinely used. The low concentrations required, together with the fact that progesterone was without effect and RU‐486 blocked the actions of dexamethasone, strongly suggest that dexamethasone acts via glucocorticoid receptors and was not acting non‐selectively via changes in membrane fluidity (Gerritsen et al , 1991), or simply by competition for LPS binding sites (TahriJouti & Chaby, 1990).…”

Section: Discussionmentioning

confidence: 99%

“…concentrations routinely used. The low concentrations required, together with the fact that progesterone was without eect and RU-486 blocked the actions of dexamethasone, strongly suggest that dexamethasone acts via glucocorticoid receptors and was not acting non-selectively via changes in membrane¯uidity (Gerritsen et al, 1991), or simply by competition for LPS binding sites (TahriJouti & Chaby, 1990). Further studies established that dexamethasone acted via the induction of LC1, since pre-perfusion of hearts with the anti-LC1 neutralizing antibody LCPS1 markedly attenuated the inhibitory actions of dexamethasone.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of acute vasodilator response to bacterial lipopolysaccharide in the rat coronary microcirculation

Cannon

Mann

Baydoun

1998

British J Pharmacology

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1 In this study the mechanisms of the acute vasodilator action of bacterial lipopolysaccharide (LPS) were investigated in the rat Langendor perfused heart. 2 Infusion of LPS (5 mg ml 71) caused a rapid and sustained fall in coronary perfusion pressure (PP) of 59+4 mmHg (n=12) and a biphasic increase in NO levels determined in the coronary euent by chemiluminescent detection. Both the fall in PP and the increase in NO release were completely abolished (n=3) by pretreatment of hearts with the NO synthase inhibitor L-NAME (50 mM). 3 LPS-induced vasodilatation was markedly attenuated to 5+4 mmHg (n=3) by pretreatment of hearts with the B 2 kinin receptor antagonist Hoe-140 (100 nM). 4 Vasodilator responses to LPS were also blocked by brief pretreatment with mepacrine (0.5 mM, n=3) or nordihydroguaiaretic acid (0.1 mM, n=4) and markedly attenuated by WEB 2086 (3 mM, n=4). 5 Thirty minutes pretreatment of hearts with dexamethasone (1 nM), but not progesterone (1 mM), signi®cantly modi®ed responses to LPS. The action of dexamethasone was time-dependent, having no eect when applied either simultaneously with or pre-perfused for 5 min before the administration of LPS but inhibiting the response to LPS by 91+1% (n=4) when pre-perfused for 15 min. The inhibition caused by dexamethasone was blocked by 15 min pretreatment with the glucocorticoid receptor antagonist RU-486 (100 nM) or by 2 min pre-perfusion of a 1 : 200 dilution of LCPS1, a selective antilipocortin 1 (LC1) neutralizing antibody. 6 Treatment with the protein synthesis inhibitor, cycloheximide (10 mM, for 15 min) selectively blunted LPS-induced vasodilatation, reducing the latter to 3+5 mmHg (n=3), while having no eect on vasodilator responses to either bradykinin or sodium nitroprusside. 7 These results indicate that LPS-induced vasodilatation in the rat heart is dependent on activation of kinin B 2 receptors and synthesis of NO. In addition, phospholipase A 2 (PLA 2 ) is activated by LPS resulting in the release of platelet-activating factor (PAF) and lipoxygenase but not cyclo-oxygenase products. These eects are dependent on de novo synthesis of an intermediate protein which remains to be identi®ed.

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Specific binding of lipopolysaccharides to mouse macrophages—I. Characteristics of the interaction and inefficiency of the polysaccharide region

Cited by 25 publications

References 53 publications

Bacterial endotoxin rapidly stimulates prolonged endothelium‐dependent vasodilatation in the rat isolated perfused heart

Bacterial endotoxin rapidly stimulates prolonged endothelium‐dependent vasodilatation in the rat isolated perfused heart

An Essential Role for Albumin in the Interaction of Endotoxin with Lipopolysaccharide-binding Protein and sCD14 and Resultant Cell Activation

Mechanisms of acute vasodilator response to bacterial lipopolysaccharide in the rat coronary microcirculation

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