These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Dermal exposure determines the outcome of repeated airway exposure in a long-term chemical-induced asthma-like mouse model.
    Author: Pollaris L, Van Den Broucke S, Decaesteker T, Cremer J, Seys S, Devos FC, Provoost S, Maes T, Verbeken E, Vande Velde G, Nemery B, Hoet PHM, Vanoirbeek JAJ.
    Journal: Toxicology; 2019 Jun 01; 421():84-92. PubMed ID: 31071364.
    Abstract:
    BACKGROUND: Exposure to diisocyanates is an important cause of occupational asthma (OA) in the industrialized world. Since OA occurs after long-term exposure to diisocyanates, we developed a chronic mouse model of chemical-induced asthma where toluene diisocyanate (TDI) was administered at two different exposure sites. OBJECTIVES: Evaluating the effect of long-term respiratory isocyanate exposure - with or without prior dermal exposure- on sensitization, inflammatory responses and airway hyperreactivity (AHR). METHODS: On days 1 and 8, BALB/c mice were dermally treated (20 μl/ear) with 0.5% 2,4-toluene diisocyanate TDI or the vehicle acetone olive oil (AOO) (3:2). Starting from day 15, mice received intranasal instillations with 0.1% TDI of vehicle five times in a week, for five successive weeks. One day after the last instillation airway hyperreactivity (AHR) to methacholine was assessed, followed by an evaluation of pulmonary inflammation and structural lung changes. Immune-related parameters were assessed in the lungs (BAL and tissue), blood, cervical- and auricular lymph nodes. RESULTS: Mice repeatedly intranasally exposed to TDI showed systemic sensitization and a mixed Th1/Th2 type immune response, without the presence of AHR. However, when mice are first dermally sensitized with TDI, followed by repeated intranasal TDI challenges, this results in a pronounced Th2 response and AHR. CONCLUSION: Dermal exposure to TDI determines airway hyperreactivity after repeated airway exposure to TDI.
    [Abstract] [Full Text] [Related] [New Search]