Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation

Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the ef...
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Autor*in:	Qiu-Meng Xie [verfasserIn] Ning Chen [verfasserIn] Si-Ming Song [verfasserIn] Cui-Cui Zhao [verfasserIn] Ya Ruan [verfasserIn] Jia-Feng Sha [verfasserIn] Qian Liu [verfasserIn] Xu-Qin Jiang [verfasserIn] Guang-He Fei [verfasserIn] Hui-Mei Wu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	allergic airway inflammation itaconate Irg1 alveolar macrophage mitochondrial NLRP3 inflammasome

Übergeordnetes Werk:	In: Antioxidants - MDPI AG, 2013, 12(2023), 2, p 489
Übergeordnetes Werk:	volume:12 ; year:2023 ; number:2, p 489

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/antiox12020489

Katalog-ID:	DOAJ081024088

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allfields	10.3390/antiox12020489 doi (DE-627)DOAJ081024088 (DE-599)DOAJ6fd9baf345d54be1a916f8361a71c4c1 DE-627 ger DE-627 rakwb eng RM1-950 Qiu-Meng Xie verfasserin aut Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects of the Irg1/itaconate pathway on AAI and alveolar macrophage (AM) immune responses were evaluated using an ovalbumin (OVA)-induced AAI model established by wild type (WT) and <i<Irg1</i<<sup<−/−</sup< mice, while the mechanism of this process was investigated by metabolomics analysis, mitochondrial/cytosolic protein fractionation and transmission electron microscopy in the lung tissues. The results demonstrated that the <i<Irg1</i< mRNA/protein expression and itaconate production in the lung were significantly induced by OVA. Itaconate ameliorated while <i<Irg1</i< deficiency augmented AAI, and this may be attributed to the fact that itaconate suppressed mitochondrial events such as NLRP3 inflammasome activation, oxidative stress and metabolic dysfunction. Furthermore, we identified that the Irg1/itaconate pathway impacted the NLRP3 inflammasome activation and oxidative stress in AMs. Collectively, our findings provide evidence for the first time, supporting the conclusion that in the allergic lung, the itaconate level is markedly increased, which directly regulates AMs’ immune responses. We therefore propose that the Irg1/itaconate pathway in AMs is a potential anti-inflammatory and anti-oxidative therapeutic target for AAI. allergic airway inflammation itaconate Irg1 alveolar macrophage mitochondrial NLRP3 inflammasome Therapeutics. Pharmacology Ning Chen verfasserin aut Si-Ming Song verfasserin aut Cui-Cui Zhao verfasserin aut Ya Ruan verfasserin aut Jia-Feng Sha verfasserin aut Qian Liu verfasserin aut Xu-Qin Jiang verfasserin aut Guang-He Fei verfasserin aut Hui-Mei Wu verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 2, p 489 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:2, p 489 https://doi.org/10.3390/antiox12020489 kostenfrei https://doaj.org/article/6fd9baf345d54be1a916f8361a71c4c1 kostenfrei https://www.mdpi.com/2076-3921/12/2/489 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_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 12 2023 2, p 489
spelling	10.3390/antiox12020489 doi (DE-627)DOAJ081024088 (DE-599)DOAJ6fd9baf345d54be1a916f8361a71c4c1 DE-627 ger DE-627 rakwb eng RM1-950 Qiu-Meng Xie verfasserin aut Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects of the Irg1/itaconate pathway on AAI and alveolar macrophage (AM) immune responses were evaluated using an ovalbumin (OVA)-induced AAI model established by wild type (WT) and <i<Irg1</i<<sup<−/−</sup< mice, while the mechanism of this process was investigated by metabolomics analysis, mitochondrial/cytosolic protein fractionation and transmission electron microscopy in the lung tissues. The results demonstrated that the <i<Irg1</i< mRNA/protein expression and itaconate production in the lung were significantly induced by OVA. Itaconate ameliorated while <i<Irg1</i< deficiency augmented AAI, and this may be attributed to the fact that itaconate suppressed mitochondrial events such as NLRP3 inflammasome activation, oxidative stress and metabolic dysfunction. Furthermore, we identified that the Irg1/itaconate pathway impacted the NLRP3 inflammasome activation and oxidative stress in AMs. Collectively, our findings provide evidence for the first time, supporting the conclusion that in the allergic lung, the itaconate level is markedly increased, which directly regulates AMs’ immune responses. We therefore propose that the Irg1/itaconate pathway in AMs is a potential anti-inflammatory and anti-oxidative therapeutic target for AAI. allergic airway inflammation itaconate Irg1 alveolar macrophage mitochondrial NLRP3 inflammasome Therapeutics. Pharmacology Ning Chen verfasserin aut Si-Ming Song verfasserin aut Cui-Cui Zhao verfasserin aut Ya Ruan verfasserin aut Jia-Feng Sha verfasserin aut Qian Liu verfasserin aut Xu-Qin Jiang verfasserin aut Guang-He Fei verfasserin aut Hui-Mei Wu verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 2, p 489 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:2, p 489 https://doi.org/10.3390/antiox12020489 kostenfrei https://doaj.org/article/6fd9baf345d54be1a916f8361a71c4c1 kostenfrei https://www.mdpi.com/2076-3921/12/2/489 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_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 12 2023 2, p 489
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allfieldsGer	10.3390/antiox12020489 doi (DE-627)DOAJ081024088 (DE-599)DOAJ6fd9baf345d54be1a916f8361a71c4c1 DE-627 ger DE-627 rakwb eng RM1-950 Qiu-Meng Xie verfasserin aut Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects of the Irg1/itaconate pathway on AAI and alveolar macrophage (AM) immune responses were evaluated using an ovalbumin (OVA)-induced AAI model established by wild type (WT) and <i<Irg1</i<<sup<−/−</sup< mice, while the mechanism of this process was investigated by metabolomics analysis, mitochondrial/cytosolic protein fractionation and transmission electron microscopy in the lung tissues. The results demonstrated that the <i<Irg1</i< mRNA/protein expression and itaconate production in the lung were significantly induced by OVA. Itaconate ameliorated while <i<Irg1</i< deficiency augmented AAI, and this may be attributed to the fact that itaconate suppressed mitochondrial events such as NLRP3 inflammasome activation, oxidative stress and metabolic dysfunction. Furthermore, we identified that the Irg1/itaconate pathway impacted the NLRP3 inflammasome activation and oxidative stress in AMs. Collectively, our findings provide evidence for the first time, supporting the conclusion that in the allergic lung, the itaconate level is markedly increased, which directly regulates AMs’ immune responses. We therefore propose that the Irg1/itaconate pathway in AMs is a potential anti-inflammatory and anti-oxidative therapeutic target for AAI. allergic airway inflammation itaconate Irg1 alveolar macrophage mitochondrial NLRP3 inflammasome Therapeutics. Pharmacology Ning Chen verfasserin aut Si-Ming Song verfasserin aut Cui-Cui Zhao verfasserin aut Ya Ruan verfasserin aut Jia-Feng Sha verfasserin aut Qian Liu verfasserin aut Xu-Qin Jiang verfasserin aut Guang-He Fei verfasserin aut Hui-Mei Wu verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 2, p 489 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:2, p 489 https://doi.org/10.3390/antiox12020489 kostenfrei https://doaj.org/article/6fd9baf345d54be1a916f8361a71c4c1 kostenfrei https://www.mdpi.com/2076-3921/12/2/489 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_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 12 2023 2, p 489
allfieldsSound	10.3390/antiox12020489 doi (DE-627)DOAJ081024088 (DE-599)DOAJ6fd9baf345d54be1a916f8361a71c4c1 DE-627 ger DE-627 rakwb eng RM1-950 Qiu-Meng Xie verfasserin aut Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects of the Irg1/itaconate pathway on AAI and alveolar macrophage (AM) immune responses were evaluated using an ovalbumin (OVA)-induced AAI model established by wild type (WT) and <i<Irg1</i<<sup<−/−</sup< mice, while the mechanism of this process was investigated by metabolomics analysis, mitochondrial/cytosolic protein fractionation and transmission electron microscopy in the lung tissues. The results demonstrated that the <i<Irg1</i< mRNA/protein expression and itaconate production in the lung were significantly induced by OVA. Itaconate ameliorated while <i<Irg1</i< deficiency augmented AAI, and this may be attributed to the fact that itaconate suppressed mitochondrial events such as NLRP3 inflammasome activation, oxidative stress and metabolic dysfunction. Furthermore, we identified that the Irg1/itaconate pathway impacted the NLRP3 inflammasome activation and oxidative stress in AMs. Collectively, our findings provide evidence for the first time, supporting the conclusion that in the allergic lung, the itaconate level is markedly increased, which directly regulates AMs’ immune responses. We therefore propose that the Irg1/itaconate pathway in AMs is a potential anti-inflammatory and anti-oxidative therapeutic target for AAI. allergic airway inflammation itaconate Irg1 alveolar macrophage mitochondrial NLRP3 inflammasome Therapeutics. Pharmacology Ning Chen verfasserin aut Si-Ming Song verfasserin aut Cui-Cui Zhao verfasserin aut Ya Ruan verfasserin aut Jia-Feng Sha verfasserin aut Qian Liu verfasserin aut Xu-Qin Jiang verfasserin aut Guang-He Fei verfasserin aut Hui-Mei Wu verfasserin aut In Antioxidants MDPI AG, 2013 12(2023), 2, p 489 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:12 year:2023 number:2, p 489 https://doi.org/10.3390/antiox12020489 kostenfrei https://doaj.org/article/6fd9baf345d54be1a916f8361a71c4c1 kostenfrei https://www.mdpi.com/2076-3921/12/2/489 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_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 12 2023 2, p 489
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authorswithroles_txt_mv	Qiu-Meng Xie @@aut@@ Ning Chen @@aut@@ Si-Ming Song @@aut@@ Cui-Cui Zhao @@aut@@ Ya Ruan @@aut@@ Jia-Feng Sha @@aut@@ Qian Liu @@aut@@ Xu-Qin Jiang @@aut@@ Guang-He Fei @@aut@@ Hui-Mei Wu @@aut@@
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callnumber-first	R - Medicine
author	Qiu-Meng Xie
spellingShingle	Qiu-Meng Xie misc RM1-950 misc allergic airway inflammation misc itaconate misc Irg1 misc alveolar macrophage misc mitochondrial misc NLRP3 inflammasome misc Therapeutics. Pharmacology Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation
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topic_title	RM1-950 Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation allergic airway inflammation itaconate Irg1 alveolar macrophage mitochondrial NLRP3 inflammasome
topic	misc RM1-950 misc allergic airway inflammation misc itaconate misc Irg1 misc alveolar macrophage misc mitochondrial misc NLRP3 inflammasome misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc allergic airway inflammation misc itaconate misc Irg1 misc alveolar macrophage misc mitochondrial misc NLRP3 inflammasome misc Therapeutics. Pharmacology
topic_browse	misc RM1-950 misc allergic airway inflammation misc itaconate misc Irg1 misc alveolar macrophage misc mitochondrial misc NLRP3 inflammasome misc Therapeutics. Pharmacology
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title	Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation
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title_full	Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation
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author_browse	Qiu-Meng Xie Ning Chen Si-Ming Song Cui-Cui Zhao Ya Ruan Jia-Feng Sha Qian Liu Xu-Qin Jiang Guang-He Fei Hui-Mei Wu
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title_sort	itaconate suppresses the activation of mitochondrial nlrp3 inflammasome and oxidative stress in allergic airway inflammation
callnumber	RM1-950
title_auth	Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation
abstract	Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects of the Irg1/itaconate pathway on AAI and alveolar macrophage (AM) immune responses were evaluated using an ovalbumin (OVA)-induced AAI model established by wild type (WT) and <i<Irg1</i<<sup<−/−</sup< mice, while the mechanism of this process was investigated by metabolomics analysis, mitochondrial/cytosolic protein fractionation and transmission electron microscopy in the lung tissues. The results demonstrated that the <i<Irg1</i< mRNA/protein expression and itaconate production in the lung were significantly induced by OVA. Itaconate ameliorated while <i<Irg1</i< deficiency augmented AAI, and this may be attributed to the fact that itaconate suppressed mitochondrial events such as NLRP3 inflammasome activation, oxidative stress and metabolic dysfunction. Furthermore, we identified that the Irg1/itaconate pathway impacted the NLRP3 inflammasome activation and oxidative stress in AMs. Collectively, our findings provide evidence for the first time, supporting the conclusion that in the allergic lung, the itaconate level is markedly increased, which directly regulates AMs’ immune responses. We therefore propose that the Irg1/itaconate pathway in AMs is a potential anti-inflammatory and anti-oxidative therapeutic target for AAI.
abstractGer	Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects of the Irg1/itaconate pathway on AAI and alveolar macrophage (AM) immune responses were evaluated using an ovalbumin (OVA)-induced AAI model established by wild type (WT) and <i<Irg1</i<<sup<−/−</sup< mice, while the mechanism of this process was investigated by metabolomics analysis, mitochondrial/cytosolic protein fractionation and transmission electron microscopy in the lung tissues. The results demonstrated that the <i<Irg1</i< mRNA/protein expression and itaconate production in the lung were significantly induced by OVA. Itaconate ameliorated while <i<Irg1</i< deficiency augmented AAI, and this may be attributed to the fact that itaconate suppressed mitochondrial events such as NLRP3 inflammasome activation, oxidative stress and metabolic dysfunction. Furthermore, we identified that the Irg1/itaconate pathway impacted the NLRP3 inflammasome activation and oxidative stress in AMs. Collectively, our findings provide evidence for the first time, supporting the conclusion that in the allergic lung, the itaconate level is markedly increased, which directly regulates AMs’ immune responses. We therefore propose that the Irg1/itaconate pathway in AMs is a potential anti-inflammatory and anti-oxidative therapeutic target for AAI.
abstract_unstemmed	Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects of the Irg1/itaconate pathway on AAI and alveolar macrophage (AM) immune responses were evaluated using an ovalbumin (OVA)-induced AAI model established by wild type (WT) and <i<Irg1</i<<sup<−/−</sup< mice, while the mechanism of this process was investigated by metabolomics analysis, mitochondrial/cytosolic protein fractionation and transmission electron microscopy in the lung tissues. The results demonstrated that the <i<Irg1</i< mRNA/protein expression and itaconate production in the lung were significantly induced by OVA. Itaconate ameliorated while <i<Irg1</i< deficiency augmented AAI, and this may be attributed to the fact that itaconate suppressed mitochondrial events such as NLRP3 inflammasome activation, oxidative stress and metabolic dysfunction. Furthermore, we identified that the Irg1/itaconate pathway impacted the NLRP3 inflammasome activation and oxidative stress in AMs. Collectively, our findings provide evidence for the first time, supporting the conclusion that in the allergic lung, the itaconate level is markedly increased, which directly regulates AMs’ immune responses. We therefore propose that the Irg1/itaconate pathway in AMs is a potential anti-inflammatory and anti-oxidative therapeutic target for AAI.
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container_issue	2, p 489
title_short	Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation
url	https://doi.org/10.3390/antiox12020489 https://doaj.org/article/6fd9baf345d54be1a916f8361a71c4c1 https://www.mdpi.com/2076-3921/12/2/489 https://doaj.org/toc/2076-3921
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Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation

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