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      Anti-Inflammatory Effect of Wasp Venom in BV-2 Microglial Cells in Comparison with Bee Venom

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          Abstract

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          As the population of the yellow-legged hornet ( Vespa velutina) spreads, this study investigated ways to utilize this resource of abundant invasive wasp species. Hymenoptera venoms, including bee venom and wasp venom, have therapeutic potential. Although the venoms are toxic to humans, the elucidation of their composition and working mechanisms has led to discoveries about their potential applications in treatment modalities for a variety of disorders. Therefore, we examined the anti-inflammatory effect of wasp venom from V. velutina in comparison with that of bee venom from honey bee on BV-2 murine microglial cells. Treatment with wasp venom reduced the secretion of nitric oxide and pro-inflammatory cytokines, including interleukin-6 and tumor necrosis factor alpha, from BV-2 cells activated by lipopolysaccharide (LPS). Western blot analysis revealed that wasp venom and bee venom decreased the expression levels of inflammation markers, including inducible nitric oxide synthase and cyclooxygenase-2. In addition, wasp venom decreased the nuclear translocation of nuclear factor κB (NF-κB), which is a key transcription factor in the regulation of cellular inflammatory response. Overall, the findings demonstrated that wasp venom inhibited LPS-induced inflammation in microglial cells by suppressing the NF-κB-mediated signaling pathway, which warrants further studies to confirm its therapeutic potential for neurodegenerative diseases.

          Abstract

          The aim of this study was to compare the anti-inflammatory effect of wasp venom (WV) from the yellow-legged hornet ( Vespa velutina) with that of bee venom (BV) on BV-2 murine microglial cells. WV was collected from the venom sac, freeze-dried, and used for in vitro examinations. WV and BV were non-toxic to BV-2 cells at concentrations of 160 and 12 µg/mL or lower, respectively. Treatment with WV reduced the secretion of nitric oxide and proinflammatory cytokines, including interleukin-6 and tumor necrosis factor alpha, from BV-2 cells activated by lipopolysaccharide (LPS). Western blot analysis revealed that WV and BV decreased the expression levels of inflammation markers, including inducible nitric oxide synthase and cyclooxygenase-2. In addition, WV decreased the nuclear translocation of nuclear factor κB (NF-κB), which is a key transcription factor in the regulation of cellular inflammatory response. Cumulatively, the results demonstrated that WV inhibited LPS-induced neuroinflammation in microglial cells by suppressing the NF-κB-mediated signaling pathway, which warrants further studies to confirm its therapeutic potential for neurodegenerative diseases.

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          Most cited references 75

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          Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism.

          Inflammation, a common denominator among the diverse list of neurodegenerative diseases, has recently been implicated as a critical mechanism responsible for the progressive nature of neurodegeneration. Microglia are the resident innate immune cells in the central nervous system and produce a barrage of factors (IL-1, TNFalpha, NO, PGE2, superoxide) that are toxic to neurons. Evidence supports that the unregulated activation of microglia in response to environmental toxins, endogenous proteins, and neuronal death results in the production of toxic factors that propagate neuronal injury. In the following review, we discuss the common thread of microglial activation across numerous neurodegenerative diseases, define current perceptions of how microglia are damaging neurons, and explain how the microglial response to neuronal damage results in a self-propelling cycle of neuron death.
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            Microglia and non-parenchymal macrophages in the brain are mononuclear phagocytes that are increasingly recognized to be essential players in the development, homeostasis and diseases of the central nervous system. With the availability of new genetic, molecular and pharmacological tools, considerable advances have been made towards our understanding of the embryonic origins, developmental programmes and functions of these cells. These exciting discoveries, some of which are still controversial, also raise many new questions, which makes brain macrophage biology a fast-growing field at the intersection of neuroscience and immunology. Here, we review the current knowledge of how and where brain macrophages are generated, with a focus on parenchymal microglia. We also discuss their normal functions during development and homeostasis, the disturbance of which may lead to various neurodegenerative and neuropsychiatric diseases.
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              Inflammation in neurodegenerative disease--a double-edged sword.

              Inflammation is a defense reaction against diverse insults, designed to remove noxious agents and to inhibit their detrimental effects. It consists of a dazzling array of molecular and cellular mechanisms and an intricate network of controls to keep them in check. In neurodegenerative diseases, inflammation may be triggered by the accumulation of proteins with abnormal conformations or by signals emanating from injured neurons. Given the multiple functions of many inflammatory factors, it has been difficult to pinpoint their roles in specific (patho)physiological situations. Studies of genetically modified mice and of molecular pathways in activated glia are beginning to shed light on this issue. Altered expression of different inflammatory factors can either promote or counteract neurodegenerative processes. Since many inflammatory responses are beneficial, directing and instructing the inflammatory machinery may be a better therapeutic objective than suppressing it.
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                Author and article information

                Contributors
                Role: Academic Editor
                Role: Academic Editor
                Journal
                Insects
                Insects
                insects
                Insects
                MDPI
                2075-4450
                29 March 2021
                April 2021
                : 12
                : 4
                Affiliations
                [1 ]School of Food Science and Biotechnology, Kyungpook National University, Daegu 41566, Korea; solideo0116@ 123456naver.com
                [2 ]Institute of Agriculture Science and Technology, Kyungpook National University, Daegu 41566, Korea; j.oh@ 123456knu.ac.kr (J.O.); lzsunny@ 123456daum.net (J.S.L.)
                [3 ]National Institute for Korean Medicine Development, Gyeongsan 38540, Korea; indersee31@ 123456nikom.or.kr
                Author notes
                [* ]Correspondence: vision@ 123456knu.ac.kr ; Tel.: +82-53-950-5752; Fax: +82-53-950-6750
                [†]

                These authors contributed equally to this work.

                Article
                insects-12-00297
                10.3390/insects12040297
                8066097
                33805372
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

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