Preventive and therapeutic effect of anti-IL-17 in an experimental model of elastase-induced lung injury in C57Bl6 mice

被引:7
作者
Fukuzaki, Silvia [1 ]
Righetti, Renato Fraga [1 ,2 ]
dos Santos, Tabata Maruyama [1 ,2 ]
Camargo, Leandro do Nascimento [1 ,2 ]
Aristoteles, Luciana R. C. R. B. [1 ]
Souza, Flavia C. R. [1 ]
Garrido, Aurelio C. [1 ]
Saraiva-Romanholo, Beatriz Mangueira [1 ,3 ]
Leick, Edna Aparecida [1 ]
Prado, Carla Maximo [1 ,4 ]
Martins, Milton de Arruda [1 ]
Lopes Calvo Tiberio, Iolanda de Fatima [1 ]
机构
[1] Univ Sao Paulo, Sch Med, Fac Med, Sao Paulo, SP, Brazil
[2] Hosp Sirio Libanes, Sao Paulo, Brazil
[3] Univ City Sao Paulo, Hosp Publ Employee Sao Paulo, Dept Med LIM 20, Inst Assistencia Med Servidor Publ Estadual Sao P, Sao Paulo, Brazil
[4] Univ Fed Sao Paulo, Dept Biosci, Santos, SP, Brazil
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 2021年 / 320卷 / 03期
基金
巴西圣保罗研究基金会;
关键词
airway remodeling; inflammation; interleukin-17; pancreatic elastase; pulmonary emphysema; MATRIX METALLOPROTEINASES; EXTRACELLULAR-MATRIX; INDUCED SPUTUM; TISSUE-REPAIR; INFLAMMATION; COPD; EMPHYSEMA; DISEASE; EXACERBATIONS; EXPRESSION;
D O I
10.1152/ajpcell.00017.2020
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Chronic obstructive pulmonary disease (COPD) is an important health care issue, and IL-17 can modulate inflammatory responses. We evaluated preventive and therapeutic effect of anti-interleukin (IL)-17 in a model of lung injury induced by elastase, using 32 male C57Bl6 mice, divided into 4 groups: SAL, ELASTASE CONTROL (EC), ELASTASE I PREVENTIVE ANTI-IL-17 (EP), and ELASTASE + THERAPEUTIC ANTI-IL-17 (ET). On the 29th day, animals were anesthetized with thiopental, tracheotomized, and placed on a ventilator to evaluate lung mechanical, exhaled nitric oxide (eNO), and total cells of bronchoalveolar lavage fluid was collected. We performed histological techniques, and linear mean intercept (Lm) was analyzed. Both treatments with anti-IL-17 decreased respiratory resistance and elastance, airway resistance, elastance of pulmonary parenchyma, eNO, and Lm compared with EC. There was reduction in total cells and macrophages in ET compared with EC. Both treatments decreased nuclear factor-kappa B, inducible nitric oxide synthase, matrix metalloproteinase (MMP)-9, MMP-12, transforming growth factor-beta, tumor necrosis factor-alpha, neutrophils, IL-1 beta, isoprostane, and IL-17 in airways and alveolar septa; collagen fibers, decorin and lumican in airways; and elastic fibers and fibronectin in alveolar septa compared with EC. There was reduction of collagen fibers in alveolar septa and biglycan in airways in EP and a reduction of eNO synthase in airways in ET. In conclusion, both treatments with anti-IL-17 contributed to improve most of parameters evaluated in inflammation and extracellular matrix remodeling in this model of lung injury.
引用
收藏
页码:C341 / C354
页数:14
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