Corrigendum: Complement System Inhibition Modulates the Pro-Inflammatory Effects of a Snake Venom Metalloproteinase

Luchini, Lygia Samartin Gonçalves; Pidde, Giselle; Squaiella-Baptistão, Carla Cristina; Tambourgi, Denise V.

doi:10.3389/fimmu.2019.01539

Cited by 4 publications

(3 citation statements)

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“…Additionally, venoms can have detrimental effects on platelet function and components of the complement system (94,95). In particular, snake venoms can trigger critical pathologies, such as venom-induced consumption, thrombocytopenia, and hemorrhage (94,95).…”

Section: Chemical Mediatorsmentioning

confidence: 99%

Immunological Responses to Envenomation

et al. 2021

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Venoms are complex mixtures of toxic compounds delivered by bite or sting. In humans, the consequences of envenomation range from self-limiting to lethal. Critical host defence against envenomation comprises innate and adaptive immune strategies targeted towards venom detection, neutralisation, detoxification, and symptom resolution. In some instances, venoms mediate immune dysregulation that contributes to symptom severity. This review details the involvement of immune cell subtypes and mediators, particularly of the dermis, in host resistance and venom-induced immunopathology. We further discuss established venom-associated immunopathology, including allergy and systemic inflammation, and investigate Irukandji syndrome as a potential systemic inflammatory response. Finally, this review characterises venom-derived compounds as a source of immune modulating drugs for treatment of disease.

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Section: Chemical Mediatorsmentioning

confidence: 99%

Immunological Responses to Envenomation

et al. 2021

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“…Importantly, the digestion products of metalloproteases can be biologically active: these bioactive peptides affect tissue growth, remodeling, repair and development [42]. In addition, these bioactive peptides increase venom toxicity by triggering and amplifying inflammation [15]. Further, they induce the transcription and translation of endogenous matrix metalloproteases that attack types of collagen that are outside the range of svMPs [41].…”

Section: Venom Translocation From Circulation To Interstitial Compartmentioning

confidence: 99%

“…These mediators, in combination with cytokines and chemokines, trigger various clinical and pathologic features of inflammation, including edema, pain, chemotaxis, cytokine release, and leukocyte activation. In addition, hyaluronidase, glycosylated proteins and svMPs promote different aspects of inflammation, which includes a range of effects, including complement activation [15].…”

Section: Inflammation and Inflammation-mediatedmentioning

confidence: 99%

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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