Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase
Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and...
Ausführliche Beschreibung
Autor*in: |
Kwang-Sik Lee [verfasserIn] Bo-Yeon Kim [verfasserIn] Min-Ji Park [verfasserIn] Yijie Deng [verfasserIn] Jin-Myung Kim [verfasserIn] Yun-Hui Kim [verfasserIn] Eun-Jee Heo [verfasserIn] Hyung-Joo Yoon [verfasserIn] Kyeong-Yong Lee [verfasserIn] Yong-Soo Choi [verfasserIn] Byung-Rae Jin [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2022 |
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Schlagwörter: |
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Übergeordnetes Werk: |
In: Toxins - MDPI AG, 2010, 14(2022), 8, p 558 |
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Übergeordnetes Werk: |
volume:14 ; year:2022 ; number:8, p 558 |
Links: |
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DOI / URN: |
10.3390/toxins14080558 |
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Katalog-ID: |
DOAJ084994495 |
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10.3390/toxins14080558 doi (DE-627)DOAJ084994495 (DE-599)DOAJ41dc98113b3f41e7853ec358ec9a266b DE-627 ger DE-627 rakwb eng Kwang-Sik Lee verfasserin aut Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and its functional link to the acute inflammatory response has not been determined to date. Here, we confirmed that SOD3 in bee venom (bvSOD3) acts as an inducer of H<sub<2</sub<O<sub<2</sub< production to promote acute inflammatory responses. In mouse models, exogenous bvSOD3 rapidly induced H<sub<2</sub<O<sub<2</sub< overproduction through superoxides that are endogenously produced by melittin and phospholipase A<sub<2</sub<, which then upregulated caspase-1 activation and proinflammatory molecule secretion and promoted an acute inflammatory response. We also showed that the relatively severe noxious effect of bvSOD3 elevated a type 2 immune response and bvSOD3 immunization protected against venom-induced inflammation. Our findings provide a novel view of the mechanism underlying bee venom-induced acute inflammation and offer a new approach to therapeutic treatments for bee envenoming and bee venom preparations for venom therapy/immunotherapy. bee venom arthropod venom envenoming superoxide dismutase hydrogen peroxide acute inflammation Medicine R Bo-Yeon Kim verfasserin aut Min-Ji Park verfasserin aut Yijie Deng verfasserin aut Jin-Myung Kim verfasserin aut Yun-Hui Kim verfasserin aut Eun-Jee Heo verfasserin aut Hyung-Joo Yoon verfasserin aut Kyeong-Yong Lee verfasserin aut Yong-Soo Choi verfasserin aut Byung-Rae Jin verfasserin aut In Toxins MDPI AG, 2010 14(2022), 8, p 558 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:14 year:2022 number:8, p 558 https://doi.org/10.3390/toxins14080558 kostenfrei https://doaj.org/article/41dc98113b3f41e7853ec358ec9a266b kostenfrei https://www.mdpi.com/2072-6651/14/8/558 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2022 8, p 558 |
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10.3390/toxins14080558 doi (DE-627)DOAJ084994495 (DE-599)DOAJ41dc98113b3f41e7853ec358ec9a266b DE-627 ger DE-627 rakwb eng Kwang-Sik Lee verfasserin aut Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and its functional link to the acute inflammatory response has not been determined to date. Here, we confirmed that SOD3 in bee venom (bvSOD3) acts as an inducer of H<sub<2</sub<O<sub<2</sub< production to promote acute inflammatory responses. In mouse models, exogenous bvSOD3 rapidly induced H<sub<2</sub<O<sub<2</sub< overproduction through superoxides that are endogenously produced by melittin and phospholipase A<sub<2</sub<, which then upregulated caspase-1 activation and proinflammatory molecule secretion and promoted an acute inflammatory response. We also showed that the relatively severe noxious effect of bvSOD3 elevated a type 2 immune response and bvSOD3 immunization protected against venom-induced inflammation. Our findings provide a novel view of the mechanism underlying bee venom-induced acute inflammation and offer a new approach to therapeutic treatments for bee envenoming and bee venom preparations for venom therapy/immunotherapy. bee venom arthropod venom envenoming superoxide dismutase hydrogen peroxide acute inflammation Medicine R Bo-Yeon Kim verfasserin aut Min-Ji Park verfasserin aut Yijie Deng verfasserin aut Jin-Myung Kim verfasserin aut Yun-Hui Kim verfasserin aut Eun-Jee Heo verfasserin aut Hyung-Joo Yoon verfasserin aut Kyeong-Yong Lee verfasserin aut Yong-Soo Choi verfasserin aut Byung-Rae Jin verfasserin aut In Toxins MDPI AG, 2010 14(2022), 8, p 558 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:14 year:2022 number:8, p 558 https://doi.org/10.3390/toxins14080558 kostenfrei https://doaj.org/article/41dc98113b3f41e7853ec358ec9a266b kostenfrei https://www.mdpi.com/2072-6651/14/8/558 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2022 8, p 558 |
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10.3390/toxins14080558 doi (DE-627)DOAJ084994495 (DE-599)DOAJ41dc98113b3f41e7853ec358ec9a266b DE-627 ger DE-627 rakwb eng Kwang-Sik Lee verfasserin aut Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and its functional link to the acute inflammatory response has not been determined to date. Here, we confirmed that SOD3 in bee venom (bvSOD3) acts as an inducer of H<sub<2</sub<O<sub<2</sub< production to promote acute inflammatory responses. In mouse models, exogenous bvSOD3 rapidly induced H<sub<2</sub<O<sub<2</sub< overproduction through superoxides that are endogenously produced by melittin and phospholipase A<sub<2</sub<, which then upregulated caspase-1 activation and proinflammatory molecule secretion and promoted an acute inflammatory response. We also showed that the relatively severe noxious effect of bvSOD3 elevated a type 2 immune response and bvSOD3 immunization protected against venom-induced inflammation. Our findings provide a novel view of the mechanism underlying bee venom-induced acute inflammation and offer a new approach to therapeutic treatments for bee envenoming and bee venom preparations for venom therapy/immunotherapy. bee venom arthropod venom envenoming superoxide dismutase hydrogen peroxide acute inflammation Medicine R Bo-Yeon Kim verfasserin aut Min-Ji Park verfasserin aut Yijie Deng verfasserin aut Jin-Myung Kim verfasserin aut Yun-Hui Kim verfasserin aut Eun-Jee Heo verfasserin aut Hyung-Joo Yoon verfasserin aut Kyeong-Yong Lee verfasserin aut Yong-Soo Choi verfasserin aut Byung-Rae Jin verfasserin aut In Toxins MDPI AG, 2010 14(2022), 8, p 558 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:14 year:2022 number:8, p 558 https://doi.org/10.3390/toxins14080558 kostenfrei https://doaj.org/article/41dc98113b3f41e7853ec358ec9a266b kostenfrei https://www.mdpi.com/2072-6651/14/8/558 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2022 8, p 558 |
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10.3390/toxins14080558 doi (DE-627)DOAJ084994495 (DE-599)DOAJ41dc98113b3f41e7853ec358ec9a266b DE-627 ger DE-627 rakwb eng Kwang-Sik Lee verfasserin aut Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and its functional link to the acute inflammatory response has not been determined to date. Here, we confirmed that SOD3 in bee venom (bvSOD3) acts as an inducer of H<sub<2</sub<O<sub<2</sub< production to promote acute inflammatory responses. In mouse models, exogenous bvSOD3 rapidly induced H<sub<2</sub<O<sub<2</sub< overproduction through superoxides that are endogenously produced by melittin and phospholipase A<sub<2</sub<, which then upregulated caspase-1 activation and proinflammatory molecule secretion and promoted an acute inflammatory response. We also showed that the relatively severe noxious effect of bvSOD3 elevated a type 2 immune response and bvSOD3 immunization protected against venom-induced inflammation. Our findings provide a novel view of the mechanism underlying bee venom-induced acute inflammation and offer a new approach to therapeutic treatments for bee envenoming and bee venom preparations for venom therapy/immunotherapy. bee venom arthropod venom envenoming superoxide dismutase hydrogen peroxide acute inflammation Medicine R Bo-Yeon Kim verfasserin aut Min-Ji Park verfasserin aut Yijie Deng verfasserin aut Jin-Myung Kim verfasserin aut Yun-Hui Kim verfasserin aut Eun-Jee Heo verfasserin aut Hyung-Joo Yoon verfasserin aut Kyeong-Yong Lee verfasserin aut Yong-Soo Choi verfasserin aut Byung-Rae Jin verfasserin aut In Toxins MDPI AG, 2010 14(2022), 8, p 558 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:14 year:2022 number:8, p 558 https://doi.org/10.3390/toxins14080558 kostenfrei https://doaj.org/article/41dc98113b3f41e7853ec358ec9a266b kostenfrei https://www.mdpi.com/2072-6651/14/8/558 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2022 8, p 558 |
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10.3390/toxins14080558 doi (DE-627)DOAJ084994495 (DE-599)DOAJ41dc98113b3f41e7853ec358ec9a266b DE-627 ger DE-627 rakwb eng Kwang-Sik Lee verfasserin aut Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and its functional link to the acute inflammatory response has not been determined to date. Here, we confirmed that SOD3 in bee venom (bvSOD3) acts as an inducer of H<sub<2</sub<O<sub<2</sub< production to promote acute inflammatory responses. In mouse models, exogenous bvSOD3 rapidly induced H<sub<2</sub<O<sub<2</sub< overproduction through superoxides that are endogenously produced by melittin and phospholipase A<sub<2</sub<, which then upregulated caspase-1 activation and proinflammatory molecule secretion and promoted an acute inflammatory response. We also showed that the relatively severe noxious effect of bvSOD3 elevated a type 2 immune response and bvSOD3 immunization protected against venom-induced inflammation. Our findings provide a novel view of the mechanism underlying bee venom-induced acute inflammation and offer a new approach to therapeutic treatments for bee envenoming and bee venom preparations for venom therapy/immunotherapy. bee venom arthropod venom envenoming superoxide dismutase hydrogen peroxide acute inflammation Medicine R Bo-Yeon Kim verfasserin aut Min-Ji Park verfasserin aut Yijie Deng verfasserin aut Jin-Myung Kim verfasserin aut Yun-Hui Kim verfasserin aut Eun-Jee Heo verfasserin aut Hyung-Joo Yoon verfasserin aut Kyeong-Yong Lee verfasserin aut Yong-Soo Choi verfasserin aut Byung-Rae Jin verfasserin aut In Toxins MDPI AG, 2010 14(2022), 8, p 558 (DE-627)610604236 (DE-600)2518395-3 20726651 nnns volume:14 year:2022 number:8, p 558 https://doi.org/10.3390/toxins14080558 kostenfrei https://doaj.org/article/41dc98113b3f41e7853ec358ec9a266b kostenfrei https://www.mdpi.com/2072-6651/14/8/558 kostenfrei https://doaj.org/toc/2072-6651 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2022 8, p 558 |
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Kwang-Sik Lee @@aut@@ Bo-Yeon Kim @@aut@@ Min-Ji Park @@aut@@ Yijie Deng @@aut@@ Jin-Myung Kim @@aut@@ Yun-Hui Kim @@aut@@ Eun-Jee Heo @@aut@@ Hyung-Joo Yoon @@aut@@ Kyeong-Yong Lee @@aut@@ Yong-Soo Choi @@aut@@ Byung-Rae Jin @@aut@@ |
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Kwang-Sik Lee misc bee venom misc arthropod venom misc envenoming misc superoxide dismutase misc hydrogen peroxide misc acute inflammation misc Medicine misc R Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase |
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Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase bee venom arthropod venom envenoming superoxide dismutase hydrogen peroxide acute inflammation |
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bee venom induces acute inflammation through a h<sub<2</sub<o<sub<2</sub<-mediated system that utilizes superoxide dismutase |
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Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase |
abstract |
Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and its functional link to the acute inflammatory response has not been determined to date. Here, we confirmed that SOD3 in bee venom (bvSOD3) acts as an inducer of H<sub<2</sub<O<sub<2</sub< production to promote acute inflammatory responses. In mouse models, exogenous bvSOD3 rapidly induced H<sub<2</sub<O<sub<2</sub< overproduction through superoxides that are endogenously produced by melittin and phospholipase A<sub<2</sub<, which then upregulated caspase-1 activation and proinflammatory molecule secretion and promoted an acute inflammatory response. We also showed that the relatively severe noxious effect of bvSOD3 elevated a type 2 immune response and bvSOD3 immunization protected against venom-induced inflammation. Our findings provide a novel view of the mechanism underlying bee venom-induced acute inflammation and offer a new approach to therapeutic treatments for bee envenoming and bee venom preparations for venom therapy/immunotherapy. |
abstractGer |
Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and its functional link to the acute inflammatory response has not been determined to date. Here, we confirmed that SOD3 in bee venom (bvSOD3) acts as an inducer of H<sub<2</sub<O<sub<2</sub< production to promote acute inflammatory responses. In mouse models, exogenous bvSOD3 rapidly induced H<sub<2</sub<O<sub<2</sub< overproduction through superoxides that are endogenously produced by melittin and phospholipase A<sub<2</sub<, which then upregulated caspase-1 activation and proinflammatory molecule secretion and promoted an acute inflammatory response. We also showed that the relatively severe noxious effect of bvSOD3 elevated a type 2 immune response and bvSOD3 immunization protected against venom-induced inflammation. Our findings provide a novel view of the mechanism underlying bee venom-induced acute inflammation and offer a new approach to therapeutic treatments for bee envenoming and bee venom preparations for venom therapy/immunotherapy. |
abstract_unstemmed |
Venoms from venomous arthropods, including bees, typically induce an immediate local inflammatory response; however, how venoms acutely elicit inflammatory response and which components induce an inflammatory response remain unknown. Moreover, the presence of superoxide dismutase (SOD3) in venom and its functional link to the acute inflammatory response has not been determined to date. Here, we confirmed that SOD3 in bee venom (bvSOD3) acts as an inducer of H<sub<2</sub<O<sub<2</sub< production to promote acute inflammatory responses. In mouse models, exogenous bvSOD3 rapidly induced H<sub<2</sub<O<sub<2</sub< overproduction through superoxides that are endogenously produced by melittin and phospholipase A<sub<2</sub<, which then upregulated caspase-1 activation and proinflammatory molecule secretion and promoted an acute inflammatory response. We also showed that the relatively severe noxious effect of bvSOD3 elevated a type 2 immune response and bvSOD3 immunization protected against venom-induced inflammation. Our findings provide a novel view of the mechanism underlying bee venom-induced acute inflammation and offer a new approach to therapeutic treatments for bee envenoming and bee venom preparations for venom therapy/immunotherapy. |
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Bee Venom Induces Acute Inflammation through a H<sub<2</sub<O<sub<2</sub<-Mediated System That Utilizes Superoxide Dismutase |
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