Lipopolysaccharide-binding protein is present in effluents of patients with Gram-negative and Gram-positive CAPD peritonitis

Schäfer, Katrin; Schumann, R.; Stöteknuel, S; Schollmeyer, P.; Dobos, Gustav

doi:10.1093/ndt/13.4.969

Cited by 11 publications

(6 citation statements)

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“…On the other hand, it was reported that in the presence of LBP the expression of pro‐inflammatory cytokines, such as IL‐1 β , IL‐6 and TNF‐ α , was all up‐regulated in the stimulation of LPS (Schäfer et al 1998). In contrast, an in vitro study found that IL‐1 β and cigarette smoke condensate induced the expression of LBP and CD14 by human airway epithelial cells (Regueiro et al 2009).…”

Section: Discussionmentioning

confidence: 99%

The interplay of lipopolysaccharide‐binding protein and cytokines in periodontal health and disease

Ren¹,

Jiang²,

Fu³

et al. 2009

J Clinic Periodontology

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Section: Discussionmentioning

confidence: 99%

The interplay of lipopolysaccharide‐binding protein and cytokines in periodontal health and disease

Ren¹,

Jiang²,

Fu³

et al. 2009

J Clinic Periodontology

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“…Zweigner et al [11] did not analyze LBP levels in regards to survival. One study performed in patients with chronic ambulatory peritoneal dialysis has described elevated LBP serum levels in peritoneal efflux of patients suffering from gram-negative and gram-positive peritonitis [14], but no corresponding LBP serum levels were provided. Kaden et al [10] described elevated LBP serum levels in 2 patients, who had undergone kidney transplantation, with Pneumocystis carinii pneumonia complicated by mycotic superinfection.…”

Section: Discussionmentioning

confidence: 99%

“…In one study performed in patients with chronic renal failure and peritonitis secondary to gram-positive agents, increased LBP serum levels have been observed in peritoneal fluid samples, but there were no data for concomitant serum levels [14]. Kaden et al [10] have reported an increase in LBP serum levels in 2 patients with Pneumocystis carinii and mycotic superinfection, who had undergone transplantation, but no detail is available for LBP serum levels in pure my- cotic infections.…”

mentioning

confidence: 99%

Lipopolysaccharide‐Binding Protein Serum Levels in Patients with Severe Sepsis Due to Gram‐Positive and Fungal Infections

Blairon¹,

Wittebole²,

Laterre³

2003

J INFECT DIS

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Lipopolysaccharide-binding protein (LBP) is increased in patients with severe gram-negative infections, but LBP serum levels have not been reported for in patients with gram-positive and fungal infections. LBP serum levels were determined in patients with severe sepsis secondary to gram-positive or fungal infections and were compared with LBP serum levels obtained from patients with gram-negative mixed infections and from healthy volunteers. Thirty-seven episodes of severe sepsis were analyzed among 24 patients. LBP serum levels were significantly increased in patients with severe sepsis (46.4+/-28.3 microg/mL), compared with that of healthy volunteers (5.7+/-1.9 microg/mL; P<.0001). On the other hand, LBP serum levels obtained from patients with gram-negative infections (40.80+/-34.79 microg/mL) did not differ from those obtained from patients with gram-positive (35.55+/-23.95 microg/mL) or fungal (39.90+/-22.19 microg/mL) infections. These data suggest that LBP is an aspecific marker of sepsis, and the response was not clearly correlated with severity. Furthermore, in patients with multiple episodes of sepsis, LBP response seems to be of lesser magnitude after each subsequent episode of severe sepsis.

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“…Thus, as for LPS, these factors include LPS-binding protein (LBP), which is synthesized mainly in hepatocytes and secreted into the bloodstream constitutively in small amounts (1 g/ml in mice) or in larger amounts (5 g/ml) as a class I acute-phase protein induced hours after challenge (37). Indeed, the concentration of this protein is minimal in uninflamed peritoneal fluid in vivo, although its abundant presence in inflamed peritoneal fluid in vivo (35) and its necessity for LPS activation of (murine) peritoneal macrophages have been demonstrated in vitro (15). LBP catalyzes the monomerization of LPS micelles and transfers the monomers as LPS-LBP complexes to another protein, CD14.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Mouse Endotoxic Fever by Complement

Holers

Boackle

et al. 2002

Infect Immun

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It was recently reported that the complement system may be critically involved in the febrile response of guinea pigs to systemic, particularly intraperitoneally (i.p.) injected, lipopolysaccharides (LPS). The present study was designed to identify which component(s) of the complement cascade may be specifically critical. To this end, we used mice with C3, C5, and CR2 gene deletions. To assess preliminarily the suitability of mice for such a study, we replicated our earlier studies with guinea pigs. Thus, to verify initially whether complement is similarly involved in the febrile response of wild-type (C57BL/6J) mice to i.p. LPS (Escherichia coli, 1 g/mouse), we depleted complement with cobra venom factor (CVF; 7 U/mouse, intravenously [i.v.]). These animals did not develop fever, whereas the core temperature (T c ) of CVF vehicle-treated controls rose ϳ1°C by 80 min postinjection and then gradually abated over the following 2.5 h, confirming the involvement of complement in fever production after i.p. LPS injection and the suitability of this species for these studies. C3-and C5-sufficient (C3 ؉/؉ and C5 ؉/؉ ) mice also developed 1°C fevers within 80 min after i.p. LPS (1 or 2 g/mouse) injection. These fevers were totally prevented by CVF (10 U/mouse, i.v.) pretreatment. C3-and C5-deficient (C3 ؊/؊ and C5 ؊/؊ ) mice were also unable to develop T c rises after i.p. LPS. Both CR2 ؉/؉ and CR2 ؊/؊ mice responded normally to i.p. LPS (1 g/mouse). These data indicate that C5, but not C3d acting through CR2, may play a critical role in the febrile response of mice to i.p. LPS.

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Lipopolysaccharide-binding protein is present in effluents of patients with Gram-negative and Gram-positive CAPD peritonitis

Cited by 11 publications

References 0 publications

The interplay of lipopolysaccharide‐binding protein and cytokines in periodontal health and disease

The interplay of lipopolysaccharide‐binding protein and cytokines in periodontal health and disease

Lipopolysaccharide‐Binding Protein Serum Levels in Patients with Severe Sepsis Due to Gram‐Positive and Fungal Infections

Modulation of Mouse Endotoxic Fever by Complement

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