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Metabolic signaling functions of the heme oxygenase/CO system in metabolic diseases

Cellular & Molecular Immunology 2018年第12期15卷 1085-1087页

作者： Hyo Jeong Kim yeonsoo joe Young-Joon Surh Hun Taeg Chung Department of Biological Sciences University of UlsanUlsanSouth Korea Tumor Microenvironment Global Core Research Center Research Institute of Pharmaceutical SciencesSeoul National UniversitySeoulSouth Korea

Immunometabolism is the intersection of immunology and *** heme oxygenase(HO)-1 and carbon monoxide(CO)(HO-1/CO)system can be induced by various stresses,including infection,and its function is to relieve stresses such as oxidative and inflammatory *** we demonstrate that the HO-1/CO system is intimately involved in the beneficial modulation of metabolic pathways via the production of ATF4 through an integrative stress response.

关键词： system monoxide oxidative

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IRG1 induced by heme oxygenase- 1/carbon monoxide inhibits LPS-mediated sepsis and pro-inflammatory cytokine production

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Cellular & Molecular Immunology 2016年第2期13卷 170-179页

作者： Md Jamal Uddin yeonsoo joe Seul-Ki Kim Sun Oh Jeong Stefan W Ryter Hyun-Ock Pae Hun Taeg Chung School of Biological Sciences University of Ulsan Korea Department of Microbiology and Immunology Wonkwang University School of Medicine Korea Joan and Sanford I. Weill Department of Medicine New York-Presbyterian Hospital Weill Cornell Medical College New York USA

The immunoresponsive gene 1 （IRG 1） protein has crucial functions in embryonic implantation and neurodegeneration. IRG1 promotes endotoxin tolerance by increasing A20 expression in macrophages through reactive oxygen species （ROS）. The cytoprotective protein heme oxygenase-1 （HO-1）, which generates endogenous carbon monoxide （CO）, is expressed in the lung during Lipopolysaccharide （LPS） tolerance and cross tolerance. However, the detailed molecular mechanisms and functional links between IRG1 and HO-1 in the innate immune system remain unknown. In the present study, we found that the CO releasing molecule-2 （CORM-2） and chemical inducers of HO- 1 increased I RG 1 expression in a time- and dose-dependent fashion in RAW264.7 cells. Furthermore, inhibition of HO-1 activity by zinc protoporphyrin IX （ZnPP） and HO-1 siRNA significantly reduced expression of IRG1 under these conditions. In addition, treatment with CO and HO-1 induction significantly increased A20 expression, which was reversed by ZnPP and HO-1 siRNA. LPS-stimulated TNF-a was significantly decreased, whereas IRG1 and A20 were increased by CORM-2 application and HO-1 induction, which in turn were abrogated by ZnPP. Interestingly, siRNA against IRG1 and A20 reversed the effects of CO and HO-1 on LPS-stimulated TNF-a production. Additionally, CO and HO-1 inducers significantly increased IRG1 and A20 expression and downregulated TNF-a production in a LPS-stimulated sepsis mice model. Furthermore, the effects of CO and HO-1 on TNF-α production were significantly reversed when ZnPP was administered. In conclusion, CO and HO-1 induction regulates IRG1 and A20 expression, leading to inhibition of inflammation in vitroand in an in vivomice model.

关键词： A2O anti-inflammatory effects carbon monoxide HO-1 IRG1

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Carbon monoxide decreases interleukin-1β levels in the lung through the induction of pyrin

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Cellular & Molecular Immunology 2017年第4期14卷 349-359页

作者： Seul-Ki Kim yeonsoo joe Yingqing Chen Jinhyun Ryu Jeong-Hee Lee Gyeong Jae Cho Stefan W. Ryter Hun Taeg Chung Department of Biological Sciences University of Ulsan Ulsan 680-749 Republic of Korea Department of Anatomy School of Medicine and Institute of Health Sciences Gyeongsang National University Jinju 660-701 Republic of Korea Department of Pathology School of Medicine and Institute of Health Sciences Gyeongsang National University Jinju 660-701 Republic of Korea Joan and Sanford I. Weill Department of Medicine New York-Presbyterian Hospital Division of Pulmonary and Critical Care Medicine Weill Cornell Medical Center New York NY USA

Carbon monoxide （CO） can act as an anti-inflammatory effector in mouse models of lung injury and disease, through the downregulation of pro-inflammatory cytokines production, though the underlying mechanisms remain unclear. The nucleotide-binding oligomerization domain-, leucine-rich region-, and pyrin domain-containing-3 （NLRP3） inflammasome is a protein complex that regulates the maturation and secretion of pro-inflammatory cytokines, including interleukin-1β （IL-1β）. In this report, we show that the CO-releasing molecule （CORM-2） can stimulate the expression of pyrin, a negative regulator of the NLRP3 inflammasome. CORM-2 increased the transcription of pyrin in the human leukemic cell line （THP-1） in the absence and presence of lipopolysaccharide （LPS）. In THP-1 cells, CORM-2 treatment dose-dependently reduced the activation of caspase-1 and the secretion of IL-lp, and increased the levels of IL-IO, in response to LPS and adenosine 5＇-triphosphate （ATP）, an NLRP3 inflammasome activation model. Genetic interference of IL-10 by small interfering RNA （siRNA） reduced the effectiveness of CORM-2 in inhibiting IL-1β production and in inducing pyrin expression. Genetic interference of pyrin by siRNA increased IL-lp production in response to LPS and ATP, and reversed CORM-2-dependent inhibition of caspase-1 activation. CO inhalation （250 ppm） in vivo increased the expression of pyrin and IL-10 in lung and spleen, and decreased the levels of IL-1β induced by LPS. Consistent with the induction of pyrin and IL-10, and the downregulation of lung IL-1β production, CO provided protection in a model of acute lung injury induced by intranasal LPS administration. These results provide a novel mechanism underlying the anti-inflammatory effects of CO, involving the IL-10-dependent upregulation of pyrin expression.

关键词： anti-inflammatory effects carbon monoxide (CO) IL-1β inflammasome pyrin

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