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      Diesel exhaust particles increase nasal symptoms and IL-17A in house dust mite-induced allergic mice

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          Abstract

          Diesel exhaust particles (DEPs), traffic-related air pollutants, are considered environmental factors adversely affecting allergic diseases. However, the immunological basis for the adjuvant effects of DEP in allergic rhinitis (AR) remains unclear. Therefore, this study aimed to investigate the effect of DEP exposure on AR using a mouse model. BALB/c mice sensitized to house dust mite (HDM) were intranasally challenged with HDM in the presence and absence of DEP. Allergic symptom scores, serum total and HDM-specific immunoglobulins (Igs), eosinophil infiltration in the nasal mucosa, cytological profiles in bronchoalveolar lavage fluid (BALF), and cytokine levels in the nasal mucosa and spleen cell culture were analyzed. Mice co-exposed to HDM and DEP showed increased allergic symptom scores compared with mice exposed to HDM alone. Reduced total IgE and HDM-specific IgE and IgG1 levels, decreased eosinophil infiltration in the nasal mucosa, and increased proportion of neutrophils in BALF were found in mice co-exposed to HDM and DEP. Interleukin (IL)-17A level was found to be increased in the nasal mucosa of the co-exposure group compared with that in the HDM-exposed group. The levels of IL-4, IL-13, interferon-γ, IL-25, IL-33, and TSLP expression showed no difference between the groups with and without DEP treatment. Increased expression of IL-17A in the nasal mucosa may contribute to DEP-mediated exacerbation of AR in HDM-sensitized murine AR model.

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          Human IL-25- and IL-33-responsive type 2 innate lymphoid cells are defined by expression of CRTH2 and CD161.

          Innate lymphoid cells (ILCs) are emerging as a family of effectors and regulators of innate immunity and tissue remodeling. Interleukin 22 (IL-22)- and IL-17-producing ILCs, which depend on the transcription factor RORγt, express CD127 (IL-7 receptor α-chain) and the natural killer cell marker CD161. Here we describe another lineage-negative CD127(+)CD161(+) ILC population found in humans that expressed the chemoattractant receptor CRTH2. These cells responded in vitro to IL-2 plus IL-25 and IL-33 by producing IL-13. CRTH2(+) ILCs were present in fetal and adult lung and gut. In fetal gut, these cells expressed IL-13 but not IL-17 or IL-22. There was enrichment for CRTH2(+) ILCs in nasal polyps of chronic rhinosinusitis, a typical type 2 inflammatory disease. Our data identify a unique type of human ILC that provides an innate source of T helper type 2 (T(H)2) cytokines.
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            IL-25 induces IL-4, IL-5, and IL-13 and Th2-associated pathologies in vivo.

            We have characterized a cytokine produced by Th2 cells, designated as IL-25. Infusion of mice with IL-25 induced IL-4, IL-5, and IL-13 gene expression. The induction of these cytokines resulted in Th2-like responses marked by increased serum IgE, IgG(1), and IgA levels, blood eosinophilia, and pathological changes in the lungs and digestive tract that included eosinophilic infiltrates, increased mucus production, and epithelial cell hyperplasia/hypertrophy. In addition, our studies show that IL-25 induces Th2-type cytokine production by accessory cells that are MHC class II(high), CD11c(dull), and lineage(-). These results suggest that IL-25, derived from Th2 T cells, is capable of amplifying allergic type inflammatory responses by its actions on other cell types.
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              Outdoor air pollution and asthma

              The Lancet, 383(9928), 1581-1592
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                Author and article information

                Contributors
                handh@snu.ac.kr
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                11 August 2021
                11 August 2021
                2021
                : 11
                : 16300
                Affiliations
                [1 ]GRID grid.411725.4, ISNI 0000 0004 1794 4809, Department of Otorhinolaryngology-Head and Neck Surgery, Chungbuk National University College of Medicine, , Chungbuk National University Hospital, ; Cheongju, Korea
                [2 ]GRID grid.31501.36, ISNI 0000 0004 0470 5905, Graduate School of Medicine, , Seoul National University College of Medicine, ; Seoul, Korea
                [3 ]GRID grid.412484.f, ISNI 0000 0001 0302 820X, Department of Otorhinolaryngology-Head and Neck Surgery, Seoul National University College of Medicine, , Seoul National University Hospital, ; 101 Daehak-ro, Jongno-gu, Seoul, 03080 Korea
                [4 ]GRID grid.412484.f, ISNI 0000 0001 0302 820X, Sensory Organ Research Institute, , Seoul National University Medical Research Center, ; Seoul, Korea
                Article
                94673
                10.1038/s41598-021-94673-9
                8357916
                34381060
                522bfe25-ca6c-4907-a651-54da102f2b07
                © The Author(s) 2021

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 29 March 2021
                : 16 June 2021
                Funding
                Funded by: NATIONAL RESEARCH FOUNDATION OF KOREA
                Award ID: 2017R1D1A1B03035317
                Award Recipient :
                Funded by: SNUH Research Fund
                Award ID: 0420150820
                Award Recipient :
                Categories
                Article
                Custom metadata
                © The Author(s) 2021

                Uncategorized
                experimental models of disease,respiratory tract diseases
                Uncategorized
                experimental models of disease, respiratory tract diseases

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