Alteration of airway hyperresponsiveness and expression of MMP-9 and TIMP-1 in bronchial tissue by nebulized IFN-$gamma; in murine model of asthma*1

Lee, Y.; Kim, Yoon‐Chul; Jon, Sangyong; Kim, K.; Kim, D.; Uh, Soo‐Taek; Park, C.

doi:10.1016/j.jaci.2004.01.254

Cited by 1 publication

(1 citation statement)

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“…In this study, Pro-MMP-9 and TIMP-1 in BALF were also increased in the asthma groups compared with the control group, which was consistent in other human and animal asthma studies, suggesting that both MMP-9 and TIMP-1 contribute to tissue remodeling ( 25 - 29 ). The balance between MMP-9 and TIMP-1 may be critical in extracellular matrix remodeling.…”

Section: Discussionsupporting

confidence: 91%

Time Sequence of Airway Remodeling in a Mouse Model of Chronic Asthma: the Relation with Airway Hyperresponsiveness

Kim

Ahn

et al. 2007

J Korean Med Sci

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During the course of establishing an animal model of chronic asthma, we tried to elucidate the time sequence of airway hyperresponsiveness (AHR), airway inflammation, airway remodeling, and associated cytokines. Seven-week-old female BALB/c mice were studied as a chronic asthma model using ovalbumin (OVA). After sensitization, mice were exposed twice weekly to aerosolized OVA, and were divided into three groups depending on the duration of 4 weeks, 8 weeks, and 12 weeks. At each time point, airway responsiveness, inflammatory cells, cytokines in bronchoalveolar lavage fluids (BALF), serum OVA-specific IgE, IgG1, IgG2a, and histological examination were carried out. AHR to methacholine, increased levels of OVA-specific IgG1 and IgG2a, and goblet cell hyperplasia were continuously sustained at each time point of weeks. In contrast, we observed a time-dependent decrease in serum OVA-specific IgE, BALF eosinophils, BALF cytokines such as IL-13, transforming growth factor-beta1, and a time-dependent increase in BALF promatrix metalloproteinase-9 and peribronchial fibrosis. In this OVA-induced chronic asthma model, we observed airway remodelings as well as various cytokines and inflammatory cells being involved in different time-dependent manners. However, increased airway fibrosis did not directly correlate with a further increase in airway hyperresponsiveness.

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Section: Discussionsupporting

confidence: 91%