Abstract
Local inflammation is a well-known symptom of envenomation by snakes of the family Viperidae, attributed primarily to the phospholipase A2s, metalloproteinases and L-amino acid oxidases contained in their venom. The inflammatory effect of snake venoms has been associated with a marked increase of the cytokines IL-1β, IL-6, IL-8, IL-10 and TNF-α. To determine the impact of Vipera ammodytes ammodytes snake venom on the expression of inflammation-related genes, we incubated human U937 monocyte cells with dilutions of snake venom. Gene expression was quantified for 28 different genes using a TaqMan® Array Human Cytokine Network 96-well Plate in a RT-qPCR system. Our results have demonstrated that 1.0 μg/mL Vipera ammodytes ammodytes venom solution induces a notable change in the expression of several cytokine network genes. Among the upregulated genes, there were several that encode interleukins, interferons, and tumor necrosis factors. We further report the downregulation of three interleukin-related genes. Our findings come as supportive information for the known complex effect of snake venoms on the human cytokine network. It also provides relevant new information regarding the expression of genes that have not been previously associated with the effect of snake venoms.
Highlights
The inflammatory process represents a defense mechanism of the body against harmful pathogens, damaged cells, or irritating substances
Key Contribution: We present a Taqman Array method to simultaneously determine the effect of Vipera ammodytes ammodytes snake venom on 28 inflammation-related genes
The results show an indicative trend of downregulation for IL12B, the gene responsible for the expression of interleukin 12 subunit beta (IL-12β)
Summary
The inflammatory process represents a defense mechanism of the body against harmful pathogens, damaged cells, or irritating substances. Inflammation can take an acute or chronic form. In its acute form, five typical signs of inflammation are usually present: heat, pain, redness, swelling, and loss of function of the affected tissues or organs. Chronic inflammatory processes are characterized by a Toxins 2018, 10, 259; doi:10.3390/toxins10070259 www.mdpi.com/journal/toxins. Toxins 2018, 10, 259 continuous and simultaneous destruction and healing of affected tissues, which may lead to chronic inflammatory diseases with detrimental effects on health [1,2]. Following the initiation of acute inflammation, the affected tissues present an increased blood flow and increased permeability of blood vessels; monocytes extravasate to the affected regions and are transformed into macrophages. Macrophages form different subsets depending on the activating signals. Lipopolysaccharides (LPS), interferon gamma (IFN-γ), or interleukin 1 beta (IL-1β) activate
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