Inflammation induced by Bothrops asper venom

Teixeira, Catarina; Cury, Yara; Moreira, Vanessa; Picolo, Gisele; Cháves, Fernando

doi:10.1016/j.toxicon.2009.03.019

Cited by 96 publications

(85 citation statements)

References 77 publications

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“…Inflammation in venom-affected tissues is associated with edema, hyperalgesia, and recruitment of inflammatory cells. These effects are induced by a variety of mediators released in the tissues, including histamine, eicosanoids, nitric oxide, complement anaphylatoxins, bradykinin, and cytokines, among others [14,31]. The present investigation explores an aspect of this pathophysiology that to date has received little attention, i.e., the possible role of the exudate, generated in the tissue, as a reservoir of potent mediators in the inflammatory events characteristic of these envenomations.…”

Section: Discussionmentioning

confidence: 99%

“…One of the best described outcomes of the direct action of the SVMPs is hemorrhage, which is the result of proteolytic degradation of key extracellular matrix proteins in the host stroma and capillaries, allowing extravasation of capillary contents into the stroma [9,10,11,12]. In addition, viperid envenomation triggers an inflammatory response which likely contributes to these pathological features, as well as being involved in tissue repair and regeneration [13,14]. …”

Section: Introductionmentioning

confidence: 99%

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

Rucavado

Nicolau

Escalante

et al. 2016

Toxins

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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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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Rucavado

Nicolau

Escalante

et al. 2016

Toxins

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“…Others, such as metalloproteinases, cause capillary endothelial damage and cell apoptosis. An inflammatory response to envenomation as evidenced by increased microvascular permeability, early leucocytosis and elevations in interleukins and tumour necrosis factor2 compounds the problem of painful swelling. The cytotoxicity is similar to that seen in crotaline species in the Americas; however, in contrast with crotaline species, coagulopathy and neurotoxicity are not a typical feature of these bites.…”

Section: Introductionmentioning

confidence: 99%

Ultrasound findings in 42 patients with cytotoxic tissue damage following bites by South African snakes

2016

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“…Such a complex array of local and systemic alterations is mostly induced by the action of metalloproteinases, phospholipases A 2 (PLA 2 ) and PLA 2 homologues, and serine proteinases, among other components [12] [13] [14] [15]. These envenomations present prominent local inflammatory response, associated with the activation of innate immune mechanisms, which might contribute to the pathogenesis of tissue damage [16].…”

Section: Introductionmentioning

confidence: 99%

Envenomations by Bothrops and Crotalus Snakes Induce the Release of Mitochondrial Alarmins

et al. 2012

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Skeletal muscle necrosis is a common manifestation of viperid snakebite envenomations. Venoms from snakes of the genus Bothrops, such as that of B. asper, induce muscle tissue damage at the site of venom injection, provoking severe local pathology which often results in permanent sequelae. In contrast, the venom of the South American rattlesnake Crotalus durissus terrificus, induces a clinical picture of systemic myotoxicity, i.e., rhabdomyolysis, together with neurotoxicity. It is known that molecules released from damaged muscle might act as ‘danger’ signals. These are known as ‘alarmins’, and contribute to the inflammatory reaction by activating the innate immune system. Here we show that the venoms of B. asper and C. d. terrificus release the mitochondrial markers mtDNA (from the matrix) and cytochrome c (Cyt c) from the intermembrane space, from ex vivo mouse tibialis anterior muscles. Cyt c was released to a similar extent by the two venoms whereas B. asper venom induced the release of higher amounts of mtDNA, thus reflecting hitherto some differences in their pathological action on muscle mitochondria. At variance, injection of these venoms in mice resulted in a different time-course of mtDNA release, with B. asper venom inducing an early onset increment in plasma levels and C. d. terrificus venom provoking a delayed release. We suggest that the release of mitochondrial ‘alarmins’ might contribute to the local and systemic inflammatory events characteristic of snakebite envenomations.

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Inflammation induced by Bothrops asper venom

Cited by 96 publications

References 77 publications

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

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

Ultrasound findings in 42 patients with cytotoxic tissue damage following bites by South African snakes

Envenomations by Bothrops and Crotalus Snakes Induce the Release of Mitochondrial Alarmins

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