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Viperid Envenomation Wound Exudate Contributes to Increased Vascular Permeability via a DAMPs/TLR-4 Mediated Pathway

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Title: Viperid Envenomation Wound Exudate Contributes to Increased Vascular Permeability via a DAMPs/TLR-4 Mediated Pathway
Authors: Alexandra Rucavado, Carolina A. Nicolau, Teresa Escalante, Junho Kim, Cristina Herrera, José María Gutiérrez, Jay W. Fox
Source: Toxins, Vol 8, Iss 12, p 349 (2016)
Publisher Information: MDPI AG, 2016.
Publication Year: 2016
Collection: LCC:Medicine
Subject Terms: snake venom metalloproteinases (SVMPs), TLR4, damage associated molecular pattern molecules (DAMPs), exudate, increased vascular permeability, Medicine
More Details: Viperid snakebite envenomation is characterized by inflammatory events including increase in vascular permeability. A copious exudate is generated in tissue injected with venom, whose proteomics analysis has provided insights into the mechanisms of venom-induced tissue damage. Hereby it is reported that wound exudate itself has the ability to induce increase in vascular permeability in the skin of mice. Proteomics analysis of exudate revealed the presence of cytokines and chemokines, together with abundant damage associated molecular pattern molecules (DAMPs) resulting from both proteolysis of extracellular matrix and cellular lysis. Moreover, significant differences in the amounts of cytokines/chemokines and DAMPs were detected between exudates collected 1 h and 24 h after envenomation, thus highlighting a complex temporal dynamic in the composition of exudate. Pretreatment of mice with Eritoran, an antagonist of Toll-like receptor 4 (TLR4), significantly reduced the exudate-induced increase in vascular permeability, thus suggesting that DAMPs might be acting through this receptor. It is hypothesized that an “Envenomation-induced DAMPs cycle of tissue damage” may be operating in viperid snakebite envenomation through which venom-induced tissue damage generates a variety of DAMPs which may further expand tissue alterations.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2072-6651
Relation: http://www.mdpi.com/2072-6651/8/12/349; https://doaj.org/toc/2072-6651
DOI: 10.3390/toxins8120349
Access URL: https://doaj.org/article/d82e8b57cd564f05926f2105bcbc66de
Accession Number: edsdoj.82e8b57cd564f05926f2105bcbc66de
Database: Directory of Open Access Journals
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  Data: Toxins, Vol 8, Iss 12, p 349 (2016)
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  Data: Viperid snakebite envenomation is characterized by inflammatory events including increase in vascular permeability. A copious exudate is generated in tissue injected with venom, whose proteomics analysis has provided insights into the mechanisms of venom-induced tissue damage. Hereby it is reported that wound exudate itself has the ability to induce increase in vascular permeability in the skin of mice. Proteomics analysis of exudate revealed the presence of cytokines and chemokines, together with abundant damage associated molecular pattern molecules (DAMPs) resulting from both proteolysis of extracellular matrix and cellular lysis. Moreover, significant differences in the amounts of cytokines/chemokines and DAMPs were detected between exudates collected 1 h and 24 h after envenomation, thus highlighting a complex temporal dynamic in the composition of exudate. Pretreatment of mice with Eritoran, an antagonist of Toll-like receptor 4 (TLR4), significantly reduced the exudate-induced increase in vascular permeability, thus suggesting that DAMPs might be acting through this receptor. It is hypothesized that an “Envenomation-induced DAMPs cycle of tissue damage” may be operating in viperid snakebite envenomation through which venom-induced tissue damage generates a variety of DAMPs which may further expand tissue alterations.
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      – SubjectFull: exudate
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