916-91 Recombinant Endotoxin-binding Protein (rBPI23) Attenuates Endotoxin-induced Circulatory Changes in Humans

Winter, Robbert J. de; Möhlen, M. A. M. Von Der; Wedel, Nancy; Delemarre, Ben J.; Deventer, S. J. H. Van

doi:10.1016/0735-1097(95)91768-s

Cited by 10 publications

(12 citation statements)

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“…However, on a molar basis, this is similar to the potency of intact BPI to inhibit LPS-induced expression of the surface antigens CR1 and CR3 on human neutrophils (20). It is also similar to the potency of rBPI 23 , a recombinant modified N-terminal fragment of human BPI with preserved LPS binding activity, to inhibit tumour necrosis factor secretion and nitrite production in mouse macrophages (32).…”

Section: Discussionmentioning

confidence: 54%

“…during treatment of the infection with antibiotics (18). Thus, intact BPI or a recombinant N-terminal fragment attenuates LPSinduced neutrophil and endothelial cell activation in vitro (20,21), as well as secretion of inflammatory mediators, neutrophil activation and circulatory changes in vivo (18,22,23). BPI, or BPI analogs, may therefore be beneficial as adjunctive treatment of severe infections (24,25).…”

Section: Discussionmentioning

confidence: 99%

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Bactericidal/permeability‐increasing protein inhibits endotoxin‐induced vascular nitric oxide synthesis

Ciornei

Egesten

Engström

et al. 2002

Acta Anaesthesiol Scand

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Background: Endotoxin (lipopolysaccharide, LPS) up‐regulates inducible nitric oxide synthase (iNOS) in blood vessels during septic shock. This promotes the production of nitric oxide (NO), leading to dilation of the vessels. The aim of the study was to investigate the effects of the LPS‐binding endogenous antibiotic bactericidal/permeability‐increasing protein (BPI) on the action of LPS on the blood vessels wall and to identify possible influence on underlying NO‐related mechanisms.Methods: Isolated segments of rat thoracic aorta and cultured primary smooth muscle cells were incubated for 5–48 h in the presence of the following combinations of compounds: (a) LPS; (b) interleukin‐1β (IL‐1β); (c) BPI; (d) BPI + LPS; (e) BPI + IL‐1β or (f) neither BPI, LPS nor IL‐1β (control). After incubation of intact segments, we measured smooth muscle contraction in response to phenylephrine and accumulation of the NO end products nitrate and nitrite in surrounding medium. Western blot was used to assess the levels of inducible nitric oxide synthase (iNOS) in cultured cells.Results: Both LPS and IL‐1β decreased contractility and increased NO production, as well as iNOS. Co‐incubation with BPI attenuated all the effects of LPS but only the effects of prolonged exposure to IL‐1β in cultured cells.Conclusion: We conclude that BPI attenuates the LPS‐induced changes in vascular reactivity by inhibiting the expression of iNOS resulting in decreased NO formation and restored responsiveness to vasoconstrictors. The data suggest that BPI can prevent circulatory disturbances during Gram‐negative sepsis.

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Bactericidal/permeability‐increasing protein inhibits endotoxin‐induced vascular nitric oxide synthesis

Ciornei

Egesten

Engström

et al. 2002

Acta Anaesthesiol Scand

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“…Open-label administration of rBPI 21 to 26 children admitted to pediatric intensive care units with fulminant meningococcemia was associated with a reduced rate of mortality relative to that predicted by clinical prognostic scores, interleukin 6 levels, and the rate for historical controls (17). In addition, trauma patients with infectious complications associated with blood loss experienced a reduced incidence of pneumonia and adult respiratory distress syndrome following treatment with rBPI 21 (8).…”

Section: Clinical Applicationmentioning

confidence: 96%

A Neutrophil-Derived Anti-Infective Molecule: Bactericidal/Permeability-Increasing Protein

Levy

2000

Antimicrob Agents Chemother

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“…Administered i.v., rBPI 21 blunts LPS-induced cardiorespiratory changes and plasma cytokine and clotting responses in human volunteers injected with LPS in vivo [54][55][56]. Phase II studies of rBPI 21 suggested benefit in a number of conditions considered to feature endotoxemia, including partial hepatectomy and traumatic blood loss [9].…”

Section: Passive Administration Of Recombinant Bpi Congenersmentioning

confidence: 99%

Deficient expression of bactericidal/permeability-increasing protein in immunocompromised hosts: translational potential of replacement therapy

Palmer

Guinan

Levy

2011

Biochemical Society Transactions

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BPI (bactericidal/permeability-increasing protein) is a 55 kDa anti-infective molecule expressed in neutrophil and eosinophil granules and on some epithelial cells. BPI's high affinity for the lipid A region of endotoxin targets its opsonizing, microbicidal and endotoxin-neutralizing activities towards Gram-negative bacteria. Several immunocompromised patient populations demonstrate BPI deficiency, including newborns, those with anti-neutrophil cytoplasmic antibodies (as in cystic fibrosis and HIV infection) and those exposed to radiochemotherapy. BPI may be replenished by administering agents that induce its expression or by administration of recombinant BPI congeners, potentially shielding BPI-deficient individuals against Gram-negative bacterial infection, endotoxemia and its toxic sequelae.

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916-91 Recombinant Endotoxin-binding Protein (rBPI23) Attenuates Endotoxin-induced Circulatory Changes in Humans

Cited by 10 publications

References 0 publications

Bactericidal/permeability‐increasing protein inhibits endotoxin‐induced vascular nitric oxide synthesis

Bactericidal/permeability‐increasing protein inhibits endotoxin‐induced vascular nitric oxide synthesis

A Neutrophil-Derived Anti-Infective Molecule: Bactericidal/Permeability-Increasing Protein

Deficient expression of bactericidal/permeability-increasing protein in immunocompromised hosts: translational potential of replacement therapy

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