Analysis of wound exudates reveals differences in the patterns of tissue damage and inflammation induced by the venoms of Daboia russelii and Bothrops asper in mice

Rucavado, Alexandra; Escalante, Teresa; Kalogeropoulos, Konstantinos; Camacho, E.; Gutiérrez, José Marı́a; Fox, Jay W.

doi:10.1016/j.toxicon.2020.07.025

Cited by 10 publications

(21 citation statements)

References 44 publications

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“…In their study, Tchaou et al [ 54 ] emphasize that viper venoms are liable for 15% envenomings and bring hemorrhagic and necrotizing complications involving several organs as well as direct toxic action of the venom on the renal parenchyma [ 54 ]. In Russel viper envenoming, acute kidney damage and nephrotoxic effects have been related to Russel’s viper venom (RVV7), which can cause hemodynamic changes and primary proximal and distal renal tubular degeneration [ 36 , 54 , 55 ]. In a cell culture study with proximal tubular cells, RVV-7 led to reduced cell viability, necrosis and increased LDH while basic protein isolated from RVV-7 might induce renal tubular necrosis in mice [ 56 ].…”

Section: Methodsmentioning

confidence: 99%

“…With recognized death risk, their bites are emergencies typically leading to the following effects: local tissue damage, bleeding, coagulopathies, and shock. However, there is clinical and experimental evidence of venoms from different snakes that cause acute kidney damage [4,[33][34][35][36]. While envenoming refers to components causing neurotoxic manifestations, other other systemic manifestations are equally present [37], whose pathways are reviewed in [38].…”

Section: Snakesmentioning

confidence: 99%

“…Some studies evaluated dissimilar venom fractions in different animals and their findings point to changes in renal hemodynamics as well as proximal and distal renal tubular degeneration [33,35]. In animal studies, kinetic evaluation of urine has also proven changes in volume as well as in creatinine, microprotein and other markers of kidney damages from this venom [33,[35][36][37].…”

Section: Snakesmentioning

confidence: 99%

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Acute kidney injury caused by venomous animals: inflammatory mechanisms

Oliveira

Cardoso

Barbosa

et al. 2021

J. Venom. Anim. Toxins incl. Trop. Dis

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Either bites or stings of venomous animals comprise relevant public health problems in tropical countries. Acute kidney injury (AKI) induced by animal toxins is related to worse prognostic and outcomes. Being one the most important pathways to induce AKI following envenoming due to animal toxins, inflammation is an essential biological response that eliminates pathogenic bacteria and repairs tissue after injury. However, direct nephrotoxicity (i.e. apoptotic and necrotic mechanisms of toxins), pigmenturia (i.e. rhabdomyolysis and hemolysis), anaphylactic reactions, and coagulopathies could contribute to the renal injury. All these mechanisms are closely integrated, but inflammation is a distinct process. Hence, it is important to improve our understanding on inflammation mechanisms of these syndromes to provide a promising outlook to reduce morbidity and mortality. This literature review highlights the main scientific evidence of acute kidney injury induced by bites or stings from venomous animals and their inflammatory mechanisms. It included observational, cross-sectional, case-control and cohort human studies available up to December 2019. Descriptors were used according to Medical Subject Headings (MeSH), namely: “Acute kidney injury” or “Venom” and “Inflammation” on Medline/Pubmed and Google Scholar; “Kidney disease” or “Acute kidney injury” on Lilacs and SciELO. The present review evidenced that, among the described forms of renal inflammation, it can occur either directly or indirectly on renal cells by means of intravascular, systemic and endothelial hemolysis, activation of inflammatory pathway, as well as direct action of venom cytotoxic components on kidney structures.

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Section: Methodsmentioning

confidence: 99%

Section: Snakesmentioning

confidence: 99%

Section: Snakesmentioning

confidence: 99%

See 1 more Smart Citation

Acute kidney injury caused by venomous animals: inflammatory mechanisms

Oliveira

Cardoso

Barbosa

et al. 2021

J. Venom. Anim. Toxins incl. Trop. Dis

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“…Blister formation following SBE, particularly in the case of B. atrox, occurs well after the bite [8,9]. Generally, blisters are related to a poor local prognosis as they increase the chance of infection and necrosis [10][11][12][13]. What is unknown is why there is such a significant delay in the formation of blisters following envenoming and why it appears antivenom treatment does not seem to prevent the appearance of blisters.…”

Section: Introductionmentioning

confidence: 99%

“…These toxins have also been implicated in inflammatory reactions associated with envenomation at the onset of local tissue damage [18]. Furthermore, it is relevant that viperid venom in general and its SVMP components, in particular, can produce a wound exudate rich in damage-associated molecular patterns (DAMPs), which contribute to chemokine and cytokine production and tissue permeability [12,13,21]. As such, it is possible that this is a contributing factor by which venom and/or SVMPs may contribute to blister formation.…”

Section: Introductionmentioning

confidence: 99%

Observation of Bothrops atrox Snake Envenoming Blister Formation from Five Patients: Pathophysiological Insights

Gimenes

Sachett

Colombini

et al. 2021

Toxins

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In the Brazilian Amazon, Bothrops atrox snakebites are frequent, and patients develop tissue damage with blisters sometimes observed in the proximity of the wound. Antivenoms do not seem to impact blister formation, raising questions regarding the mechanisms underlying blister formation. Here, we launched a clinical and laboratory-based study including five patients who followed and were treated by the standard clinical protocols. Blister fluids were collected for proteomic analyses and molecular assessment of the presence of venom and antivenom. Although this was a small patient sample, there appeared to be a correlation between the time of blister appearance (shorter) and the amount of venom present in the serum (higher). Of particular interest was the biochemical identification of both venom and antivenom in all blister fluids. From the proteomic analysis of the blister fluids, all were observed to be a rich source of damage-associated molecular patterns (DAMPs), immunomodulators, and matrix metalloproteinase-9 (MMP-9), suggesting that the mechanisms by which blisters are formed includes the toxins very early in envenomation and continue even after antivenom treatment, due to the pro-inflammatory molecules generated by the toxins in the first moments after envenomings, indicating the need for local treatments with anti-inflammatory drugs plus toxin inhibitors to prevent the severity of the wounds.

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