Aprotinin Enhances the Endogenous Release of Interleukin-10 After Cardiac Operations

Hill, Gary E.; Diego, Robert P.; Stammers, Alfred H.; Huffman, Suzanne M.; Pohorecki, Roman

doi:10.1016/s0003-4975(97)01037-0

Cited by 52 publications

(18 citation statements)

References 23 publications

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“…As neutrophils and later monocytes/macrophages are recruited to the site of healing, they release both pro- (including TNF-α, IL-1, and IL-6) and anti-inflammatory (including IL-10) cytokines which coordinate the wound healing response (41, 42). Aprotinin has been shown to induce expression of anti-inflammatory cytokines, which in turn inhibit release of pro-inflammatory cytokines from both macrophages and neutrophils (41, 43).…”

Section: Discussionmentioning

confidence: 99%

“…Aprotinin has been shown to induce expression of anti-inflammatory cytokines, which in turn inhibit release of pro-inflammatory cytokines from both macrophages and neutrophils (41, 43). In addition, aprotinin inhibits expression of endothelial cell receptors for neutrophils (ICAM-1)(41, 43) and inhibits production of pro-inflammatory cytokines which attract neutrophils (44), and therefore decreases accumulation of these inflammatory cells at the site of wound healing. Previous studies by our collaborators showed an increase in anti-inflammatory macrophages (M2 phenotype) within and around microporous implants when compared to non-porous implants, and that this macrophage switch corresponded with an increased extent of porous implant vascularization (40).…”

Section: Discussionmentioning

confidence: 99%

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Proangiogenic microtemplated fibrin scaffolds containing aprotinin promote improved wound healing responses

et al. 2013

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Survival of tissue engineered constructs after implantation depends heavily on induction of a vascular response in host tissue, promoting a quick anastomosis of the cellular graft. Additionally, implanted constructs typically induce fibrous capsule formation, effectively preventing graft integration with host tissue. Previously we described the development of a high density microtemplated fibrin scaffold for cardiac tissue engineering applications with tunable degradation and mechanical properties which promoted seeded cell survival and organization in vitro (1). Scaffold degradation in vitro was controllable by addition of the serine protease inhibitor aprotinin and/or the fibrin cross-linker Factor XIII (FXIII). The goal of this study was to assess host tissue responses to these fibrin scaffold formulations by determining effects on scaffold degradation, angiogenic responses, and fibrous capsule formation in a subcutaneous implant model. Aprotinin significantly decreased scaffold degradation over 2 weeks of implantation. A significant increase in capillary infiltration of aprotinin implants was found after 1 and 2 weeks, with a significantly greater amount of capillaries reaching the interior of aprotinin scaffolds. Interestingly, after 2 weeks the aprotinin scaffolds had a significantly thinner, yet apparently more cellular fibrous capsule than unmodified scaffolds. These results indicate aprotinin not only inhibits fibrin scaffold degradation, but also induces significant responses in the host tissue. These included an angiogenic response resulting in increased vascularization of the scaffold material over a relatively short period of time. In addition, aprotinin release from scaffolds may reduce fibrous capsule formation, which could help promote improved integration of cell-seeded scaffolds with host tissue.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Proangiogenic microtemplated fibrin scaffolds containing aprotinin promote improved wound healing responses

et al. 2013

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“…Besides its well-known protective effects on platelets and its antifibrinolytic actions, some anti-inflammatory properties have been recently attributed to aprotinin, and this ability has been shown to be dose-dependent in a variety of in vitro systems [45, 46]. This suggested that actions of aprotinin include the prevention of upregulation of neutrophil CD11b integrin necessary for neutrophil adherence and degranulation, suppression of the plasma increases of the proinflammatory cytokines IL-6 and IL-8 and enhancement of the release of the anti-inflammatory cytokine IL-10 [47, 48]. Moreover, aprotinin has been shown in vitro to inhibit TNF secretion from activated macrophages by 51% and to reduce elastase release from neutrophils [49, 50].…”

Section: Discussionmentioning

confidence: 99%

Effects of Vitamin E, Pentoxifylline and Aprotinin on Light-Induced Retinal Injury

Yılmaz

Aydemir²,

Özercan³

et al. 2007

Ophthalmologica

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Purpose: A considerable amount of clinical and experimental evidence exists suggesting the involvement of reactive oxygen species (ROS) in the etiology of light-induced retinal injury. The aim of this study was to investigate the protective role of vitamin E, pentoxifylline (PTX) and aprotinin against light-induced retinal injury in guinea pigs. Methods: Thirty adult male guinea pigs were divided into 5 groups of 6 animals each. The first group was used as control. The guinea pigs were kept in cyclic light for 2 weeks before the experiments. The animals were maintained in 12-hour light-dark cycles, before and after exposure to intense white fluorescent light, for as long as 12 h and then returned to cyclic light. Groups 3–5 received intraperitoneal injections of vitamin E, PTX and aprotinin, respectively. One eye of each animal was selected for histopathological evaluation and the other for biochemical assay. Retinal malondialdehyde (MDA) levels and the thickness of the outer nuclear layers were measured. Results: The compounds had the following relationships: vitamin E more than PTX more than aprotinin in preventing light-induced retinal damage. All 3 gave significant protection against the formation of MDA. Retinas of all 3 treatment groups had been protected from light-induced injury. Conclusion: The intraperitoneal vitamin E, PTX and aprotinin supplementations may strengthen the antioxidant defense system because of decreased ROS, and these agents may play a role in treating light-induced retinal injury.

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“…5,6 Few studies have reported patient data on the potential for aprotinin to modify the inflammatory response. In a clinical setting, using different aprotinin dosages, antiinflammatory activity characterized by reduced release of tumour necrosis factor-α (TNF-α) and interleukin (IL)-6, and enhanced endogenous release of the antiinflammatory cytokine IL-10 has been reported; 7 however, there are also conflicting data. 5 -8 The present randomized, prospective clinical study was designed to evaluate and compare the risks and effects to the inflammatory response of low-and highdose aprotinin regimens.…”

Section: High-dose Aprotinin In Cardiac Surgerymentioning

confidence: 99%

Efficacy of a High-Dose Aprotinin Regimen for Reducing Transfusion Requirements and Inflammatory Responses in Adult Cardiac Surgery

et al. 2008

J Int Med Res

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This study evaluated and compared the risks and effects to the inflammatory response of low-and high-dose aprotinin regimens. Between January and June 2006, patients scheduled for cardiac surgery using cardiopulmonary bypass were enrolled and randomly allocated to either low-(n = 15) or high-dose (n = 13) aprotinin groups. The incidences of mortality and adverse events were comparable in both groups. Post-operative creatinine levels and blood loss were not significantly different between the two groups. With the exception of platelets, the counts of transfused allogenic blood products were not significantly different between the groups. Interleukin (IL)-6, IL-10, soluble tumour necrosis factor II receptor, and interferon-g levels increased in both groups compared with baseline, but no significant intergroup differences were detected. In conclusion, high-and lowdose aprotinin had similar effects in the reduction of mediastinal bleeding and attenuation of systemic inflammatory responses, and high-dose aprotinin therapy could be used without any increased adverse effects.

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Aprotinin Enhances the Endogenous Release of Interleukin-10 After Cardiac Operations

Cited by 52 publications

References 23 publications

Proangiogenic microtemplated fibrin scaffolds containing aprotinin promote improved wound healing responses

Proangiogenic microtemplated fibrin scaffolds containing aprotinin promote improved wound healing responses

Effects of Vitamin E, Pentoxifylline and Aprotinin on Light-Induced Retinal Injury

Efficacy of a High-Dose Aprotinin Regimen for Reducing Transfusion Requirements and Inflammatory Responses in Adult Cardiac Surgery

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