An overview of the immune modulating effects of enzymatic toxins from snake venoms

Burin, Sandra Mara; Menaldo, Danilo L.; Sampaio, Suely Vilela; Frantz, Fabiani Gai; Castro, Fabíola Attié de

doi:10.1016/j.ijbiomac.2017.12.101

Cited by 24 publications

(16 citation statements)

References 88 publications

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“…A number of such studies have reported increases in interleukins, PGE 2 , TNF-α, as well as changes in leukocyte populations and migration from the action of svMPs [78][79][80]. For a recent review of svMPs and immune modulation, see the review of Burin et al [17]. Additional studies are needed to clarify the mechanism of immune modulation by metalloproteases, whether it is direct signaling by cleavage products or simply exposure of basement membranes and tissue factors during the digestion of the extracellular protein matrix.…”

Section: Snake Venom Metalloprotease (Svmp)mentioning

confidence: 99%

“…However, the interaction of the immune system and snake venoms is more complex than just type II responses. As highlighted by Burin and colleagues [17], snake venom accomplishes both immune suppression and immune stimulation, with the pattern of reaction to venom snake species-specific. The potential of using these actions of venom for immune therapy and for understanding immune responses has been much discussed [88].…”

Section: Prey Response To Venoms: How Venoms Co-opt Signaling Pathwaymentioning

confidence: 99%

“…Recent studies have coalesced on the concept that svPLA 2 and svMP appear to be the most important venom components in producing inflammation [16,95]. svPLA 2 and svMP activities sidestep the usual foreign protein recognition aspect of immune activation to directly stimulate immune cells, via arachidonic acid and pro-inflammatory digestion products [17]. This creates a response disproportionate to the immediate direct immunogenicity of the venom proteins.…”

Section: Inflammation and Inflammation-mediatedmentioning

confidence: 99%

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Amplification of Snake Venom Toxicity by Endogenous Signaling Pathways

Bickler

2020

Toxins

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The active components of snake venoms encompass a complex and variable mixture of proteins that produce a diverse, but largely stereotypical, range of pharmacologic effects and toxicities. Venom protein diversity and host susceptibilities determine the relative contributions of five main pathologies: neuromuscular dysfunction, inflammation, coagulopathy, cell/organ injury, and disruption of homeostatic mechanisms of normal physiology. In this review, we describe how snakebite is not only a condition mediated directly by venom, but by the amplification of signals dysregulating inflammation, coagulation, neurotransmission, and cell survival. Although venom proteins are diverse, the majority of important pathologic events following envenoming follow from a small group of enzyme-like activities and the actions of small toxic peptides. This review focuses on two of the most important enzymatic activities: snake venom phospholipases (svPLA2) and snake venom metalloproteases (svMP). These two enzyme classes are adept at enabling venom to recruit homologous endogenous signaling systems with sufficient magnitude and duration to produce and amplify cell injury beyond what would be expected from the direct impact of a whole venom dose. This magnification produces many of the most acutely important consequences of envenoming as well as chronic sequelae. Snake venom PLA2s and MPs enzymes recruit prey analogs of similar activity. The transduction mechanisms that recruit endogenous responses include arachidonic acid, intracellular calcium, cytokines, bioactive peptides, and possibly dimerization of venom and prey protein homologs. Despite years of investigation, the precise mechanism of svPLA2-induced neuromuscular paralysis remains incomplete. Based on recent studies, paralysis results from a self-amplifying cycle of endogenous PLA2 activation, arachidonic acid, increases in intracellular Ca2+ and nicotinic receptor deactivation. When prolonged, synaptic suppression supports the degeneration of the synapse. Interaction between endothelium-damaging MPs, sPLA2s and hyaluronidases enhance venom spread, accentuating venom-induced neurotoxicity, inflammation, coagulopathy and tissue injury. Improving snakebite treatment requires new tools to understand direct and indirect effects of envenoming. Homologous PLA2 and MP activities in both venoms and prey/snakebite victim provide molecular targets for non-antibody, small molecule agents for dissecting mechanisms of venom toxicity. Importantly, these tools enable the separation of venom-specific and prey-specific pathological responses to venom.

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Section: Snake Venom Metalloprotease (Svmp)mentioning

confidence: 99%

Section: Prey Response To Venoms: How Venoms Co-opt Signaling Pathwaymentioning

confidence: 99%

Section: Inflammation and Inflammation-mediatedmentioning

confidence: 99%

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Amplification of Snake Venom Toxicity by Endogenous Signaling Pathways

Bickler

2020

Toxins

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“…Three main enzymatic proteins have been discovered in viper venom, including proteases (serine and metalloproteinases), oxidases (L-amino acid oxidases, LAAOs), and phospholipases (especially phospholipases A 2 , PLA 2 ) [ 55 ]. Hemotoxins in venom are one of the key components that cause life-threating complications, such as systemic bleeding, coagulopathy, thrombocytopenia, and hemolysis [ 56 , 57 ].…”

Section: Pathophysiology Of Venom Induced Ocular Complicationsmentioning

confidence: 99%

Venom Ophthalmia and Ocular Complications Caused by Snake Venom

Chang

Huang

Chen

et al. 2020

Toxins

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Little is known about the detailed clinical description, pathophysiology, and efficacy of treatments for ocular envenoming (venom ophthalmia) caused by venom of the spitting elapid and other snakes, as well as ocular complications caused by snake venom injection. In this paper, we review clinical information of case reports regarding venom ophthalmia and snake venom injection with associated ocular injuries in Asia, Africa, and the United States. We also review the literature of snake venom such as their compositions, properties, and toxic effects. Based on the available clinical information and animal studies, we further discuss possible mechanisms of venom ophthalmia derived from two different routes (Duvernoy’s gland in the mouth and nuchal gland in the dorsal neck) and the pathophysiology of snake venom injection induced ocular complications, including corneal edema, corneal erosion, cataract, ocular inflammation, retinal hemorrhage, acute angle closure glaucoma, as well as ptosis, diplopia, and photophobia. Finally, we discuss the appropriate first aid and novel strategies for treating venom ophthalmia and snake envenoming.

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“…Echis Coloratus venom is vigorously attacked liver causing hepatocellular damage, hemorrhage, elevation in liver enzymes and depletion in glycogen (Al-Jammaz, 2003). Venom is composed of a cocktail of biomolecules include enzymes, peptides, carbohydrates, lipids, nucleosides, amines and inorganic metal ions such as sodium, calcium, potassium, magnesium, zinc, iron, cobalt, manganese, and nickel (Burin et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

The knockout effect of low doses of gamma radiation on hepatotoxicity induced byEchis Coloratussnake venom in rats

Samy¹,

Shaaban²,

Kenawy³

et al. 2019

Preprint

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Echis Coloratus is the most medically important viper in Egypt causing several pathological effects leading to death. Gamma radiation has been used as a venom detoxifying tool in order to extend the lifespan of the immunized animals used in antivenin production process. Thus, the aim of this study is to assess the effects of increasing doses of gamma radiation on Echis Coloratus in vivo through biochemical and histological studies. The results revealed a significant increase in the levels of AST, ALT, ALP and glucose of sera collected from the rats injected with native Echis Coloratus venom compared with the non-envenomed group. On the other hand, biochemical parameters of sera of rats administrated with either 1.5 kGy or 3 kGy irradiated venom were significantly decrease compared with the native venom envenomed group at 2h, 4h and 24h post envenomation. In addition, these results were confirmed by histological studies of rats' livers. Correspondingly, the sublethal dose injection of native Echis Coloratus venom induced significant alterations in the histological architecture of liver after 2, 4 and 24 h of injection. Concurrently, the administration of both 1.5 kGy and 3 kGy gamma irradiated venom showed fewer histological alterations compared with the native group. In conclusion, the present findings support the idea of using gamma radiation as an effective venom detoxification tool.

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An overview of the immune modulating effects of enzymatic toxins from snake venoms

Cited by 24 publications

References 88 publications

Amplification of Snake Venom Toxicity by Endogenous Signaling Pathways

Amplification of Snake Venom Toxicity by Endogenous Signaling Pathways

Venom Ophthalmia and Ocular Complications Caused by Snake Venom

The knockout effect of low doses of gamma radiation on hepatotoxicity induced byEchis Coloratussnake venom in rats

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