دورية أكاديمية

Airborne pollutant ROFA enhances the allergic airway inflammation through direct modulation of dendritic cells in an uptake-dependent mechanism.

التفاصيل البيبلوغرافية
العنوان: Airborne pollutant ROFA enhances the allergic airway inflammation through direct modulation of dendritic cells in an uptake-dependent mechanism.
المؤلفون: Arantes-Costa FM; Immunoregulation Unit, Special Laboratory of Applied Toxinology, Butantan Institute, Av. Vital Brazil, 1500, Sao Paulo CEP 05503-009, SP, Brazil; Laboratório de Terapêutica Experimental (LIM20), Faculdade de Medicina da USP, Av. Dr Arnaldo, 455, Sala 1220, Sao Paulo CEP 01246-903, SP, Brazil., Grund LZ; Immunoregulation Unit, Special Laboratory of Applied Toxinology, Butantan Institute, Av. Vital Brazil, 1500, Sao Paulo CEP 05503-009, SP, Brazil., Martins MA; Laboratório de Terapêutica Experimental (LIM20), Faculdade de Medicina da USP, Av. Dr Arnaldo, 455, Sala 1220, Sao Paulo CEP 01246-903, SP, Brazil., Lima C; Immunoregulation Unit, Special Laboratory of Applied Toxinology, Butantan Institute, Av. Vital Brazil, 1500, Sao Paulo CEP 05503-009, SP, Brazil. Electronic address: carla.lima@butantan.gov.br.
المصدر: International immunopharmacology [Int Immunopharmacol] 2014 Sep; Vol. 22 (1), pp. 9-20. Date of Electronic Publication: 2014 Jun 25.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Science Country of Publication: Netherlands NLM ID: 100965259 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-1705 (Electronic) Linking ISSN: 15675769 NLM ISO Abbreviation: Int Immunopharmacol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Amsterdam ; New York : Elsevier Science, c2001-
مواضيع طبية MeSH: Asthma/*immunology , Coal Ash/*administration & dosage , Dendritic Cells/*immunology , Lung/*immunology , Particulate Matter/*administration & dosage, Animals ; Cell Differentiation ; Cell Proliferation ; Cells, Cultured ; Disease Models, Animal ; Disease Progression ; Endocytosis ; Eosinophils/immunology ; Female ; Goblet Cells/immunology ; Humans ; Interferon-gamma/metabolism ; Interleukin-5/metabolism ; Lymphocyte Activation ; Mice, Inbred BALB C ; T-Lymphocyte Subsets/immunology
مستخلص: Studies suggest that airborne pollutants are important cofactors in the exacerbation of lung diseases. The role of DC on the exacerbation of lung inflammation induced by particulate matter pollutants is unclear. We evaluated the effects of residual oil fly ash (ROFA) on the phenotype and function of bone marrow-derived dendritic cells (BMDCs) in vitro and lung dendritic cells (DCs) in vivo, and the subsequent T-cell response. In a model of asthma, exposure to ROFA exacerbated pulmonary inflammation, which was attributed to the increase of eosinophils, IL-5- and IFN-γ-producing T cells, and goblet cells as well as decreased number of Treg and pDC. However, the ROFA showed no ability to modulate the production of anaphylactic IgE. In vitro studies showed that ROFA directly induced the maturation of DCs up-regulating the expression of co-stimulatory molecules and cytokines and MMP production in an uptake-dependent and oxidative stress-dependent manner. Furthermore, ROFA-pulsed BMDC transferred to allergic mice exacerbated eosinophilic inflammation as well as promoted increased epithelial and goblet cells changes. Thus, pollutants may constitute an important and risk factor in the exacerbation of asthma with inhibition of the negative regulatory signals in the lung, with enhanced mDC activation that sustains the recruitment of effector T lymphocytes and eosinophil.
(Copyright © 2014 Elsevier B.V. All rights reserved.)
فهرسة مساهمة: Keywords: Asthma; Dendritic cell; Particulate matter; ROFA; Regulatory cell
المشرفين على المادة: 0 (Coal Ash)
0 (Interleukin-5)
0 (Particulate Matter)
82115-62-6 (Interferon-gamma)
تواريخ الأحداث: Date Created: 20140701 Date Completed: 20150511 Latest Revision: 20140801
رمز التحديث: 20240628
DOI: 10.1016/j.intimp.2014.06.020
PMID: 24975839
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-1705
DOI:10.1016/j.intimp.2014.06.020