Hypersensitivity reactions in mouse airways after a single and a repeated hapten challenge.

Autor: van Houwelingen AH; Department of Pharmacology and Pathophysiology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, The Netherlands. A.H.vanHouwelingen@pharm.uu.nl, de Jager SC, Kool M, van Heuven-Nolsen D, Kraneveld AD, Nijkamp FP
Jazyk: angličtina
Zdroj: Inflammation research : official journal of the European Histamine Research Society ... [et al.] [Inflamm Res] 2002 Feb; Vol. 51 (2), pp. 63-8.
DOI: 10.1007/BF02684001
Abstrakt: Objective and Design: In this study, we examined the effect of a single and a repeated hapten-challenge on inflammatory processes in the airways of mice undergoing a hapten-induced non-IgE mediated hypersensitivity reaction.
Methods: BALB/c mice were skin-sensitized with the hapten dinitroflourobenzene (DNFB) and intra-airway challenged with dinitrobenzene sulphonic acid (DNS). Mucosal exudation, tracheal vascular permeability, cellular accumulation, and serum murine mast cell protease (MMCP) were investigated at different time points after the first DNS-challenge and 30 min after a repeated DNS-challenge.
Results: MMCP levels in serum were increased at all time points after single challenge and repeated challenge. Increased vascular permeability as determined by Monastral blue staining, was found in the trachea of DNFB-sensitized mice after single DNS-challenge. A second exposure to DNS profoundly enhanced the Monastral blue labeling of the tracheal blood vessels of DNFB-sensitized mice. Furthermore, increased mucosal exudation and polymorphonuclear cell (PMN) accumulation were present in DNFB-sensitized mice compared to vehicle-sensitized animals after the first DNS challenge.
Conclusions: Increased mucosal exudation, vascular permeability, and PMN accumulation are prominent inflammatory features of the DNFB-induced hypersensitivity reaction in the airways. Furthermore, mast cell activation is associated with this hapten-induced hypersensitivity reaction.
Databáze: MEDLINE
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