Cigarette smoke dissociates inflammation and lung remodeling in OVA-sensitized and challenged mice

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• 作者：Deborah C. Hizume^a ; ^c ; ^{dehizume@gmail.com} ; Alessandra C. Toledo^a ; Henrique T. Moriya^d ; Beatriz M. Saraiva-Romanholo^a ; Francine M. Almeida^a ; Fernanda M. Arantes-Costa^a ; Rodolfo P. Vieira^a ; ^e ; Marisa Dolhnikoff^b ; David Itiro Kasahara^f ; Milton A. Martins^a
• 关键词：Cigarette smoke ; Cytokines ; Growth factors ; Inflammation ; Remodeling
• 刊名：Respiratory Physiology & Neurobiology
• 出版年：2012
• 期刊代码：185_15699048
• 类别：bio
• 出版时间：30 April, 2012
• 卷：181
• 期：2
• 页码：167-176
• 文件大小：1688 K

摘要

We evaluated the effects of cigarette smoke (CS) on lung inflammation and remodeling in a model of ovalbumin (OVA)-sensitized and OVA-challenged mice. Male BALB/c mice were divided into 4 groups: non-sensitized and air-exposed (control); non-sensitized and exposed to cigarette smoke (CS), sensitized and air-exposed (OVA) (50 渭g + OVA 1%3 times/week for 3 weeks) and sensitized and cigarette smoke exposed mice (OVA + CS). IgE levels were not affected by CS exposure. The increases in total bronchoalveolar fluid cells in the OVA group were attenuated by co-exposure to CS, as were the changes in IL-4, IL-5, and eotaxin levels as well as tissue elastance (p < 0.05). In contrast, only the OVA + CS group showed a significant increase in the protein expression of IFN-纬, VEGF, GM-CSF and collagen fiber content (p < 0.05). In our study, exposure to cigarette smoke in OVA-challenged mice resulted in an attenuation of pulmonary inflammation but led to an increase in pulmonary remodeling and resulted in the dissociation of airway inflammation from lung remodeling.