Inflammation Induced by Platelet-Activating Viperid Snake Venoms: Perspectives on Thromboinflammation

Teixeira, Catarina; Fernandes, C.M.; Leiguez, Elbio; Chudzinski-Tavassi, Ana Marisa

doi:10.3389/fimmu.2019.02082

Cited by 49 publications

(37 citation statements)

References 171 publications

(182 reference statements)

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“…Hemostatic and inflammatory disorders can be considered important pathophysiological effects and are associated with the effects of different components of the venom on different cellular and molecular targets. Evidence of crosstalk between coagulation and inflammation can lead to an enhancement of the effects and to greater damage (25). Thus, the present clinical study shows for the first time the association between inflammation and coagulation in patients who were victims of B. atrox snakebites.…”

Section: Discussionsupporting

confidence: 54%

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Correlating Fibrinogen Consumption and Profiles of Inflammatory Molecules in Human Envenomation's by Bothrops atrox in the Brazilian Amazon

et al. 2020

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Snakebites are considered a major public health problem worldwide. In the Amazon region of Brazil, the snake Bothrops atrox ( B. atrox ) is responsible for 90% of the bites. These bites may cause local and systemic signs from acute inflammatory reaction and hemostatic changes, and present common hemorrhagic disorders. These alterations occur due the action of hemostatically active and immunogenic toxins which are capable of triggering a wide range of hemostatic and inflammatory events. However, the crosstalk between coagulation disorders and inflammatory reaction still has gaps in snakebites. Thus, the goal of this study was to describe the relationship between the consumption of fibrinogen and the profile of inflammatory molecules (chemokines and cytokines) in evenomations by B. atrox snakebites. A prospective study was carried out with individuals who had suffered B. atrox snakebites and presented different levels of fibrinogen consumption (normal fibrinogen [NF] and hypofibrinogenemia [HF]). Seventeen patients with NF and 55 patients with HF were eligible for the study, in addition to 50 healthy controls (CG). The molecules CXCL-8, CCL-5, CXCL-9, CCL-2, CXCL-10, IL-6, TNF, IL-2, IL-10, IFN-γ, IL-4, and IL-17A were quantified in plasma using the CBA technique at three different times (pre-antivenom therapy [T0], 24 h [T1], and 48 h [T2] after antivenom therapy). The profile of the circulating inflammatory response is different between the groups studied, with HF patients having higher concentrations of CCL-5 and lower IFN-γ. In addition, antivenom therapy seems to have a positive effect, leading to a profile of circulating inflammatory response similar in quantification of T1 and T2 on both groups. Furthermore, these results suggest that a number of interactions of CXCL-8, CXCL-9, CCL-2, IL-6, and IFN-γ in HF patients are directly affected by fibrinogen levels, which may be related to the inflammatory response and coagulation mutual relationship induced by B. atrox venom. The present study is the first report on inflammation-coagulation crosstalk involving snakebite patients and supports the better understanding of envenomation's pathophysiology mechanisms and guides in the search for novel biomarkers and prospective therapies.

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Section: Discussionsupporting

confidence: 54%

“…However, the crosstalk between coagulation disorders and inflammatory reaction still has gaps in snakebites. Current knowledge demonstrates that isolated Bothrops venom and toxins can be associated with acute inflammatory processes and coagulation disorders (25).…”

Section: Introductionmentioning

confidence: 99%

Correlating Fibrinogen Consumption and Profiles of Inflammatory Molecules in Human Envenomation's by Bothrops atrox in the Brazilian Amazon

et al. 2020

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“…LTC4 and LTD4 are a thousand times more potent than histamine, act on the smooth muscles of the peripheral respiratory tract and are bronchoconstrictor (89)(90)(91)(92). PLA2 induces inflammation with mediators' release including IL-1β, IL-6, IL-8, TNF-α, MIP-1α, NO, histamine, serotonine, PAF, bradichinine, PGE2, TXA2, LTB4, RANTES and anaphylatoxins (C3 and C5) (93).…”

Section: Discussionmentioning

confidence: 99%

The Covid-19 Virus Double Pathogenic Mechanism. A New Perspective

Brogna¹

2020

Preprint

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Acetylcholine (ACh) is the best one characterized neurotransmitter. Its central roles in the cholinergic areas and central nervous system (CNS) and peripheral (PNS) synapses are well known. It was the first molecule identified as a neurotransmitter and appears to be phylogenetically the oldest one signaling molecules. ACh was detected in bacteria, protozoa, fungi, algae and primitive plants, indicating that the cholinergic system was widely distributed in living organisms before its appearance in the nervous system. The autonomous nervous system (ANS) is an integral part animal kingdom history. It determines fight-escape reactions as well as outlining the vital and cognitive functions bio-organization rhythms. The virus (Covid-19) extraneous effects acting on it could help to better understand its functions. The Blast results show some factors like protein that can be implicated such as bungaro-toxins, phospholipase A2 and the similar prothrombin activator protein. A positive correlation with different toxins is obtained and the Covid-19 double pathogenic mechanism theory is proposed. The process allows us to outline the possibility about toxic-like factors presence.

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“…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%

“…We have described some ways that svMPs and svPLA 2 s and probably other venom components act synergistically, mediated by their biologically active products. Teixeira and colleagues have written an excellent recent review of the convergence and interaction of inflammation and coagulation disorders in snake envenoming [88]. More work is needed to uncover these important interacting mechanisms and to discover therapeutic strategies based on them.…”

Section: Interaction and Amplification Of Venom Mps And Pla 2 S In Inmentioning

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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Inflammation Induced by Platelet-Activating Viperid Snake Venoms: Perspectives on Thromboinflammation

Cited by 49 publications

References 171 publications

Correlating Fibrinogen Consumption and Profiles of Inflammatory Molecules in Human Envenomation's by Bothrops atrox in the Brazilian Amazon

Correlating Fibrinogen Consumption and Profiles of Inflammatory Molecules in Human Envenomation's by Bothrops atrox in the Brazilian Amazon

The Covid-19 Virus Double Pathogenic Mechanism. A New Perspective

Amplification of Snake Venom Toxicity by Endogenous Signaling Pathways

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