Indoleamine 2,3-Dioxygenase in Hematopoietic Stem Cell-Derived Cells Suppresses Rhinovirus-Induced Neutrophilic Airway Inflammation by Regulating Th1- and Th17-Type Responses.

Autor:	Hossain FMA; College of Veterinary Medicine and Bio-Safety Research Institute, Jeonbuk National University, Iksan 54596, Korea.; Faculty of Veterinary, Animal and Biomedical Sciences, Sylhet Agricultural University, Sylhet 3100, Bangladesh., Park SO; College of Veterinary Medicine and Bio-Safety Research Institute, Jeonbuk National University, Iksan 54596, Korea., Kim HJ; College of Veterinary Medicine and Bio-Safety Research Institute, Jeonbuk National University, Iksan 54596, Korea., Eo JC; Division of Biotechnology, College of Environmental & Biosource Science, Jeonbuk National University, Iksan 54596, Korea., Choi JY; College of Veterinary Medicine and Bio-Safety Research Institute, Jeonbuk National University, Iksan 54596, Korea., Tanveer M; College of Veterinary Medicine and Bio-Safety Research Institute, Jeonbuk National University, Iksan 54596, Korea., Uyangaa E; College of Veterinary Medicine and Bio-Safety Research Institute, Jeonbuk National University, Iksan 54596, Korea., Kim K; Department of Pharmacology, School of Medicine, Pusan National University, Yangsan 50612, Korea., Eo SK; College of Veterinary Medicine and Bio-Safety Research Institute, Jeonbuk National University, Iksan 54596, Korea.
Jazyk:	angličtina
Zdroj:	Immune network [Immune Netw] 2021 Aug 17; Vol. 21 (4), pp. e26. Date of Electronic Publication: 2021 Aug 17 (Print Publication: 2021).
DOI:	10.4110/in.2021.21.e26
Abstrakt:	Asthma exacerbations are a major cause of intractable morbidity, increases in health care costs, and a greater progressive loss of lung function. Asthma exacerbations are most commonly triggered by respiratory viral infections, particularly with human rhinovirus (hRV). Respiratory viral infections are believed to affect the expression of indoleamine 2,3-dioxygenase (IDO), a limiting enzyme in tryptophan catabolism, which is presumed to alter asthmatic airway inflammation. Here, we explored the detailed role of IDO in the progression of asthma exacerbations using a mouse model for asthma exacerbation caused by hRV infection. Our results reveal that IDO is required to prevent neutrophilic inflammation in the course of asthma exacerbation caused by an hRV infection, as corroborated by markedly enhanced Th17- and Th1-type neutrophilia in the airways of IDO-deficient mice. This neutrophilia was closely associated with disrupted expression of tight junctions and enhanced expression of inflammasome-related molecules and mucin-inducing genes. In addition, IDO ablation enhanced allergen-specific Th17- and Th1-biased CD4 + T-cell responses following hRV infection. The role of IDO in attenuating Th17- and Th1-type neutrophilic airway inflammation became more apparent in chronic asthma exacerbations after repeated allergen exposures and hRV infections. Furthermore, IDO enzymatic induction in leukocytes derived from the hematopoietic stem cell (HSC) lineage appeared to play a dominant role in attenuating Th17- and Th1-type neutrophilic inflammation in the airway following hRV infection. Therefore, IDO activity in HSC-derived leukocytes is required to regulate Th17- and Th1-type neutrophilic inflammation in the airway during asthma exacerbations caused by hRV infections. Competing Interests: Conflict of Interest: The authors declare no potential conflicts of interest. (Copyright © 2021. The Korean Association of Immunologists.)
Databáze:	MEDLINE
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