Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring
Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biol...
Ausführliche Beschreibung
Autor*in: |
Shimizu Y [verfasserIn] Tsukada T [verfasserIn] Sakata-Haga H [verfasserIn] Sakai D [verfasserIn] Shoji H [verfasserIn] Saikawa Y [verfasserIn] Hatta T [verfasserIn] |
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Englisch |
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2021 |
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In: Journal of Inflammation Research - Dove Medical Press, 2009, (2021), Seite 355-365 |
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Übergeordnetes Werk: |
year:2021 ; pages:355-365 |
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DOAJ052675572 |
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(DE-627)DOAJ052675572 (DE-599)DOAJ8a08ca48d8b84b49b1e84447ff1d4143 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Shimizu Y verfasserin aut Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biology, Kanazawa Medical University, Uchinada, Ishikawa, JapanCorrespondence: Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, JapanTel +81-76-281-8113Fax +81-76-218-8189Email thattakanazawa-med.ac.jpBackground: A number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3– 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.Results: The serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.Conclusion: Overall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.Keywords: maternal immune activation, liver necrosis, immune overreaction, unfolded protein response defects maternal immune activation liver necrosis immune overreaction unfolded protein response defects Pathology Therapeutics. Pharmacology Tsukada T verfasserin aut Sakata-Haga H verfasserin aut Sakai D verfasserin aut Shoji H verfasserin aut Saikawa Y verfasserin aut Hatta T verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2021), Seite 355-365 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2021 pages:355-365 https://doaj.org/article/8a08ca48d8b84b49b1e84447ff1d4143 kostenfrei https://www.dovepress.com/exposure-to-maternal-immune-activation-causes-congenital-unfolded-prot-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 2021 355-365 |
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(DE-627)DOAJ052675572 (DE-599)DOAJ8a08ca48d8b84b49b1e84447ff1d4143 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Shimizu Y verfasserin aut Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biology, Kanazawa Medical University, Uchinada, Ishikawa, JapanCorrespondence: Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, JapanTel +81-76-281-8113Fax +81-76-218-8189Email thattakanazawa-med.ac.jpBackground: A number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3– 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.Results: The serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.Conclusion: Overall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.Keywords: maternal immune activation, liver necrosis, immune overreaction, unfolded protein response defects maternal immune activation liver necrosis immune overreaction unfolded protein response defects Pathology Therapeutics. Pharmacology Tsukada T verfasserin aut Sakata-Haga H verfasserin aut Sakai D verfasserin aut Shoji H verfasserin aut Saikawa Y verfasserin aut Hatta T verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2021), Seite 355-365 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2021 pages:355-365 https://doaj.org/article/8a08ca48d8b84b49b1e84447ff1d4143 kostenfrei https://www.dovepress.com/exposure-to-maternal-immune-activation-causes-congenital-unfolded-prot-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 2021 355-365 |
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(DE-627)DOAJ052675572 (DE-599)DOAJ8a08ca48d8b84b49b1e84447ff1d4143 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Shimizu Y verfasserin aut Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biology, Kanazawa Medical University, Uchinada, Ishikawa, JapanCorrespondence: Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, JapanTel +81-76-281-8113Fax +81-76-218-8189Email thattakanazawa-med.ac.jpBackground: A number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3– 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.Results: The serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.Conclusion: Overall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.Keywords: maternal immune activation, liver necrosis, immune overreaction, unfolded protein response defects maternal immune activation liver necrosis immune overreaction unfolded protein response defects Pathology Therapeutics. Pharmacology Tsukada T verfasserin aut Sakata-Haga H verfasserin aut Sakai D verfasserin aut Shoji H verfasserin aut Saikawa Y verfasserin aut Hatta T verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2021), Seite 355-365 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2021 pages:355-365 https://doaj.org/article/8a08ca48d8b84b49b1e84447ff1d4143 kostenfrei https://www.dovepress.com/exposure-to-maternal-immune-activation-causes-congenital-unfolded-prot-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 2021 355-365 |
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(DE-627)DOAJ052675572 (DE-599)DOAJ8a08ca48d8b84b49b1e84447ff1d4143 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Shimizu Y verfasserin aut Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biology, Kanazawa Medical University, Uchinada, Ishikawa, JapanCorrespondence: Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, JapanTel +81-76-281-8113Fax +81-76-218-8189Email thattakanazawa-med.ac.jpBackground: A number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3– 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.Results: The serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.Conclusion: Overall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.Keywords: maternal immune activation, liver necrosis, immune overreaction, unfolded protein response defects maternal immune activation liver necrosis immune overreaction unfolded protein response defects Pathology Therapeutics. Pharmacology Tsukada T verfasserin aut Sakata-Haga H verfasserin aut Sakai D verfasserin aut Shoji H verfasserin aut Saikawa Y verfasserin aut Hatta T verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2021), Seite 355-365 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2021 pages:355-365 https://doaj.org/article/8a08ca48d8b84b49b1e84447ff1d4143 kostenfrei https://www.dovepress.com/exposure-to-maternal-immune-activation-causes-congenital-unfolded-prot-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 2021 355-365 |
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(DE-627)DOAJ052675572 (DE-599)DOAJ8a08ca48d8b84b49b1e84447ff1d4143 DE-627 ger DE-627 rakwb eng RB1-214 RM1-950 Shimizu Y verfasserin aut Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biology, Kanazawa Medical University, Uchinada, Ishikawa, JapanCorrespondence: Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, JapanTel +81-76-281-8113Fax +81-76-218-8189Email thattakanazawa-med.ac.jpBackground: A number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3– 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.Results: The serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.Conclusion: Overall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.Keywords: maternal immune activation, liver necrosis, immune overreaction, unfolded protein response defects maternal immune activation liver necrosis immune overreaction unfolded protein response defects Pathology Therapeutics. Pharmacology Tsukada T verfasserin aut Sakata-Haga H verfasserin aut Sakai D verfasserin aut Shoji H verfasserin aut Saikawa Y verfasserin aut Hatta T verfasserin aut In Journal of Inflammation Research Dove Medical Press, 2009 (2021), Seite 355-365 (DE-627)600306178 (DE-600)2494878-0 11787031 nnns year:2021 pages:355-365 https://doaj.org/article/8a08ca48d8b84b49b1e84447ff1d4143 kostenfrei https://www.dovepress.com/exposure-to-maternal-immune-activation-causes-congenital-unfolded-prot-peer-reviewed-article-JIR kostenfrei https://doaj.org/toc/1178-7031 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 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 2021 355-365 |
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Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3&ndash; 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. 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Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring |
abstract |
Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biology, Kanazawa Medical University, Uchinada, Ishikawa, JapanCorrespondence: Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, JapanTel +81-76-281-8113Fax +81-76-218-8189Email thattakanazawa-med.ac.jpBackground: A number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3– 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.Results: The serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.Conclusion: Overall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.Keywords: maternal immune activation, liver necrosis, immune overreaction, unfolded protein response defects |
abstractGer |
Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biology, Kanazawa Medical University, Uchinada, Ishikawa, JapanCorrespondence: Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, JapanTel +81-76-281-8113Fax +81-76-218-8189Email thattakanazawa-med.ac.jpBackground: A number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3– 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.Results: The serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.Conclusion: Overall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.Keywords: maternal immune activation, liver necrosis, immune overreaction, unfolded protein response defects |
abstract_unstemmed |
Yo Shimizu,1 Tsuyoshi Tsukada,2 Hiromi Sakata-Haga,2 Daisuke Sakai,3 Hiroki Shoji,3 Yutaka Saikawa,1 Toshihisa Hatta2 1Department of Pediatrics, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 2Department of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, Japan; 3Department of Biology, Kanazawa Medical University, Uchinada, Ishikawa, JapanCorrespondence: Toshihisa HattaDepartment of Anatomy, Kanazawa Medical University, Uchinada, Ishikawa, JapanTel +81-76-281-8113Fax +81-76-218-8189Email thattakanazawa-med.ac.jpBackground: A number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3– 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.Results: The serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.Conclusion: Overall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.Keywords: maternal immune activation, liver necrosis, immune overreaction, unfolded protein response defects |
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title_short |
Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring |
url |
https://doaj.org/article/8a08ca48d8b84b49b1e84447ff1d4143 https://www.dovepress.com/exposure-to-maternal-immune-activation-causes-congenital-unfolded-prot-peer-reviewed-article-JIR https://doaj.org/toc/1178-7031 |
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Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model.Materials and Methods: Pregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3&ndash; 4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. 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