Lipopolysaccharide (LPS) recognition in macrophages. Participation of LPS-binding protein and CD14 in LPS-induced adaptation in rabbit peritoneal exudate macrophages.

Mathison, John C.; Wolfson, E; Steinemann, Susan; Tobias, Peter S.; Ulevitch, Richard J.

doi:10.1172/jci116801

Cited by 78 publications

(33 citation statements)

References 37 publications

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“…8 -10 The present study confirmed that adhesion and extravasation are in full progress at 6 hours and that most PMNs have disappeared by day 3, as indicated by the small and variable numbers of CD14-immunoreactive cells in the intima and media. Even though the CD14 stain does not distinguish between monocytes and PMNs, 23 very few monocytes enter the collared artery, 8 unless lipoproteins are infused into the collar. 24 To investigate the functional significance of PMN infiltration, the number of circulating PMNs was raised by continuous treatment with G-CSF, starting 3 days before collaring.…”

Section: Discussionmentioning

confidence: 99%

Role of Polymorphonuclear Leukocytes in Collar-Induced Intimal Thickening in the Rabbit Carotid Artery

Put

Osselaer²,

Meyer³

et al. 1998

ATVB

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Abstract-In this study, the involvement of polymorphonuclear leukocytes (PMNs) in the development of intimal thickening was investigated. A fibromuscular intima was induced by placing a silicone collar around the rabbit carotid artery for 3 days or 2 weeks; the contralateral artery was sham operated. Rabbits received placebo treatments (groups 1 and 3), granulocyte-colony stimulating factor (group 2; G-CSF, 20, delivered by subcutaneous osmotic pumps), or an anti-CD18 monoclonal antibody (group 4; 1.5 mg/kg IV). The G-CSF treatment raised the peripheral PMN count 5-to 12-fold but had no effect on intimal thickening on day 3, 12, or 14. A single injection of anti-CD18 prevented PMN extravasation 6 hours after collar implantation without influencing intimal hyperplasia on day 14. Repeated daily administration of anti-CD18 strongly bound to CD18 on peripheral PMNs and inhibited both PMN-dependent plasma extravasation in the skin and accumulation of CD14-immunoreactive leukocytes in the intima and media. However, anti-CD18 did not suppress early intimal thickening or accumulation of ␣-smooth muscle actin-immunoreactive cells by day 3. It thus appears that the PMN influx in the intima and media evoked by the perivascular collar is of little functional relevance to the subsequent smooth muscle cell migration and intimal thickening in this model. (Arterioscler Thromb Vasc Biol. 1998;18:915-921.)

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Section: Discussionmentioning

confidence: 99%

Role of Polymorphonuclear Leukocytes in Collar-Induced Intimal Thickening in the Rabbit Carotid Artery

Put

Osselaer²,

Meyer³

et al. 1998

ATVB

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“…Likely mechanisms for the reduced responsiveness of these macrophages to LPS include defective recognition of LPS or deficiency in LPS-specific signal transduction pathways. This phenomenon was only exhibited when the cells where tolerized in the absence of LBP (Mathison et al 1993) which is an unlikely scenario in vivo.…”

Section: Lipopolysaccharide-binding Protein (Lbp) Lps-binding Proteimentioning

confidence: 97%

“…Increased expression of mCD14 (Ziegler-Heitbrock et al 1994) and sCD14 (Labeta et al 1993) is associated with the development of ET and has been described in animals and humans. Other models reported no change in mCD14 expression in humans, rabbits and mice (Mathison et al 1993;McCall et al 1993;Ziegler-Heitbrock et al 1997). In 2003, Heagy et al reported that mCD14 is not involved in the development of ET in human monocytes (Heagy et al 2003).…”

Section: Lbp and Cd14mentioning

confidence: 99%

“…In vivo, LBP is not required for the clearance of LPS but is essential for the rapid induction of an inflammatory response (TNF-α production) by LPS and gram negative bacteria (Jack et al 1997). In addition, LBP restores the ability of LPS-tolerant macrophages to respond to secondary LPS challenge (Mathison et al 1993). Likely mechanisms for the reduced responsiveness of these macrophages to LPS include defective recognition of LPS or deficiency in LPS-specific signal transduction pathways.…”

Section: Lipopolysaccharide-binding Protein (Lbp) Lps-binding Proteimentioning

confidence: 99%

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Induction and characterization of endotoxin tolerance in equine peripheral blood mononuclear cells in vitro

Frellstedt

McKenzie

Barrett

et al. 2012

Veterinary Immunology and Immunopathology

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Endotoxemia is responsible for severe illness in horses. Individuals can become unresponsive to the endotoxin molecule after an initial exposure; this phenomenon has been called developing a state of 'endotoxin tolerance' (ET). ET has been induced in horses in vivo; however, cytokine expression associated with ET has not been investigated. The purpose of this study was to develop and validate a method for inducing ET in equine peripheral blood mononuclear cells (PBMCs) in vitro, and to describe the cytokine profile which is associated with the ET.Blood was collected from 6 healthy horses and PBMCs were isolated. ET was induced by culturing cells with three concentrations of endotoxin given to induce ET, and evaluated after a second dose of endotoxin given to challenge the cells. The relative mRNA expression of IL-10 and IL-12 was measured by use of quantitative PCR.ET was induced in all cells (n=6) exposed to the 2-step endotoxin challenge. In PBMCs treated with 1.0 ng/ml of endotoxin followed by challenge with 10 ng/ml of endotoxin, the relative mRNA expression of IL-10 in tolerized cells was not different from positive control cells. In contrast, the relative mRNA expression of IL-12 in tolerized cells was decreased by 15-fold after the second endotoxin challenge compared with positive control cells.This experiment demonstrated a reliable method for the ex vivo induction of ET in equine PBMCs. A marked suppression of IL-12 production is associated with ET. The production of IL-10 was not altered in ET in our model.

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“…The identity of the LPS-recognition complex has been recently established. It is believed to be composed of TLR4 [1], the main transducer of signals from LPS, the GPI-linked receptor CD14 [2] and a small exteriorized adaptor known as MD-2 [3]. All three molecules are believed to form a stable complex during LPS signaling and, based on germ-line targeting [4][5][6], each is indispensable for LPS responses.…”

Section: Introductionmentioning

confidence: 99%

Mice expressing high levels of soluble CD14 retain LPS in the circulation and are resistant to LPS‐induced lethality

et al. 2006

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Despite significant progress in understanding the origin of soluble CD14 (sCD14), its physiological function remains largely unknown. Recent research has produced contradictory observations suggesting that sCD14 may have either beneficial or detrimental properties in protection against LPS-induced endotoxin shock. To resolve this controversy and to establish a mouse model suitable for elucidation of the functions of human CD14 (hCD14) in vivo, we generated several lines of transgenic mice bearing different copy numbers of the hCd14 transgene on a murine Cd14 -/-background. The hCD14 was entirely capable of complementing loss of mouse CD14 to mediate cellular responses to LPS. Serum levels of sCD14 in a founder with multiple copies of the transgene were several times higher than in transgenic animals with a single copy of Cd14. Furthermore, mice with high levels of hCD14 were hypo-responsive to LPS and survived a lethal dose of LPS. Further inquiry into the mechanism of the hypo-response to LPS revealed that protection is associated with the higher amounts of circulating LPS. Most of this circulating LPS can be immunoprecipitated with anti-CD14 antibodies. These results suggest that sCD14 blocks circulating LPS by limiting the amount of monocyte-bound LPS and thus reduces inflammatory responses.

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Lipopolysaccharide (LPS) recognition in macrophages. Participation of LPS-binding protein and CD14 in LPS-induced adaptation in rabbit peritoneal exudate macrophages.

Cited by 78 publications

References 37 publications

Role of Polymorphonuclear Leukocytes in Collar-Induced Intimal Thickening in the Rabbit Carotid Artery

Role of Polymorphonuclear Leukocytes in Collar-Induced Intimal Thickening in the Rabbit Carotid Artery

Induction and characterization of endotoxin tolerance in equine peripheral blood mononuclear cells in vitro

Mice expressing high levels of soluble CD14 retain LPS in the circulation and are resistant to LPS‐induced lethality

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