Bactericidal/Permeability-Increasing Protein Attenuates Systemic Inflammation and Acute Lung Injury in Porcine Lower Limb Ischemia–Reperfusion Injury

Harkin, Denis W.; D’Sa, Aires A.B. Barros; McCallion, K; Hoper, Margaret; Halliday, M. I.; Campbell, F. C.

doi:10.1097/00000658-200108000-00014

Cited by 28 publications

(30 citation statements)

References 50 publications

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“…Although serum calcium is not typically measured in limb I/R studies, changes in calcium metabolism do occur during reperfusion and this parameter may be a useful measure of metabolic regulation of the muscle [4,39]. There have been conflict- ing reports on the increase in circulating neutrophils following limb I/R [20,40]. We found a 3-to 4-fold increase in circulating PMNs in I/R-only rats after 4 h of reperfusion.…”

Section: Discussionmentioning

confidence: 72%

Protective effects of a potent c5a receptor antagonist on experimental acute limb ischemia-reperfusion in rats

Woodruff¹,

Shiels²,

Reid³

et al. 2004

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 72%

Protective effects of a potent c5a receptor antagonist on experimental acute limb ischemia-reperfusion in rats

Woodruff¹,

Shiels²,

Reid³

et al. 2004

Journal of Surgical Research

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“…Although the molecular mechanisms regulating lung injury after II/R are not fully elucidated, clinical and experimental studies suggest that ROS, complement activation, cytokine/chemokine generation, and activated neutrophils were responsible for II/R-induced lung injury [21][22][23]. Ischemia/reperfusion injury is initiated by production of ROS, which initially seem to be responsible for the generation of chemotactic activity for neutrophils.…”

Section: Discussionmentioning

confidence: 99%

Immediate but Not Delayed Postconditioning During Reperfusion Attenuates Acute Lung Injury Induced by Intestinal Ischemia/Reperfusion in Rats: Comparison with Ischemic Preconditioning

Liu

Huang

et al. 2009

Journal of Surgical Research

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“…31,53,54 While the majority of therapeutic strategies designed for treating sepsis have failed, 18 recent studies suggest that recombinant BPI protein is a promising therapeutic agent. [33][34][35][36][37][38][39][40] However, the production and purification of recombinant BPI have proved uneasy tasks, since BPI cannot be produced in the conventional Gram-negative bacterial strains and has to be produced in mammalian cell lines. 24 It is also difficult to maintain the integrity of purified full-length BPI protein due to its large molecular weight and complex structure.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, several studies have evaluated the effect of recombinant BPI protein in experimental models of sepsis and endotoxemia in rabbits, rats, pigs, and mice. [31][32][33][34][35][36] Furthermore, phase 1/2/3 clinical trials using recombinant BPI have been performed or are currently under way. 32,[37][38][39][40] In most cases, the regimen entails a continuous infusion of 2 to 8 mg/kg recombinant BPI for a period of 2 days.…”

mentioning

confidence: 99%

Protection from endotoxemia by adenoviral-mediated gene transfer of human bactericidal/permeability-increasing protein

Alexander

Bramson

Foley

et al. 2004

Blood

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Sepsis represents a growing concern in high-risk patients and there has been a lack of effective preventives and therapies. Bacterial/permeability increasing protein (BPI) is a human neutrophil granule-associated defense molecule specific for Gram-negative bacteria and their products. To develop a BPI-transgene-based prophylactic or therapeutic modality, we have developed a recombinant, replication-deficient adenoviral vector expressing full-length human BPI protein (Adh- BPI IntroductionSepsis is a heterogeneous condition with approximately 400 000 to 500 000 cases presented in the United States annually. 1,2 The mortality rate for all septic episodes is estimated between 30% to 50%, and approximately 70% of all septic episodes involve Gram-negative bacteria. 2,3 The Centers for Disease Control and Prevention has reported an increase in the incidence of sepsis over the last decade, which can be attributed to an increase in the number of patients at high risk for developing sepsis. 1 High-risk patients include those who are immunocompromised from HIV infection, undergoing cancer therapy, or on immunosuppressive drugs, and those undergoing invasive surgical procedures. These patients are at greater risk of exposure to bacteria, especially in the clinical setting. 4 The goal of sepsis management is to reduce or control the detrimental systemic inflammation responses to the infection using support therapies, while treatment therapies, such as antibiotics, attempt to eliminate the infection. 5 With the increase in incidence of both drug-resistant bacteria and immunocompromised septic patients, current aggressive therapies are ineffective or even detrimental, and new therapies must be developed to increase the survival of septic patients. 5-9 Moreover, it may be possible to prophylactically reduce the number of sepsis-induced mortalities by introducing a set of criteria to identify and treat high-risk individuals prior to surgery or cancer therapy.Various novel sepsis therapies currently under development or under evaluation in clinical trials include anticoagulant therapy, therapies directed at the neutralization of lipopolysaccharide (LPS), and cytokine therapies. Anticoagulant therapy aims to improve multiple organ failure by attenuating intravascular coagulation. 10 In this regard, the use of recombinant activated protein C has been shown to increase survival of patients. 10,11 However, activated protein C therapy addresses only one portion of the complex sepsis condition and does not address the important initial proinflammatory cytokine cascade elicited by LPS from Gram-negative bacteria. On the other hand, while therapies directed at the neutralization of proinflammatory cytokines, such as tumor necrosis factor ␣ (TNF-␣), are promising in experimental models, they are largely ineffective in clinical trials. 12-17 The interleukin-10 (IL-10) cytokine therapy aiming to counter the expression and effect of TNF-␣ has also proved ineffective. 18 Such cytokine therapies are thus unlikely to be the best strategy. Seps...

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Bactericidal/Permeability-Increasing Protein Attenuates Systemic Inflammation and Acute Lung Injury in Porcine Lower Limb Ischemia–Reperfusion Injury

Cited by 28 publications

References 50 publications

Protective effects of a potent c5a receptor antagonist on experimental acute limb ischemia-reperfusion in rats

Protective effects of a potent c5a receptor antagonist on experimental acute limb ischemia-reperfusion in rats

Immediate but Not Delayed Postconditioning During Reperfusion Attenuates Acute Lung Injury Induced by Intestinal Ischemia/Reperfusion in Rats: Comparison with Ischemic Preconditioning

Protection from endotoxemia by adenoviral-mediated gene transfer of human bactericidal/permeability-increasing protein

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