Effect of aging on sputum inflammation and asthma control.

Effect of aging on sputum inflammation and asthma control.
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DOI:
10.1016/j.jaci.2016.09.015
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发表时间:
2017-06
期刊:
The Journal of allergy and clinical immunology
影响因子:
--
通讯作者:
Wisnivesky JP
Wisnivesky JP
中科院分区:
其他
文献类型:
--
作者:
Busse PJ;Birmingham JM;Calatroni A;Manzi J;Goryachokovsky A;Fontela G;Federman AD;Wisnivesky JP

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老年哮喘患者的发病率和死亡率增加。关于衰老对气道炎症和哮喘控制的影响的知识有限。比较老年与年轻患者的气道炎症及其与哮喘控制的关系,并确定差异是哮喘特异性的还是由于“炎症老化”。老年(>60岁)和年轻(21-40岁)城市中心哮喘患者的前瞻性研究。在控制吸入性皮质类固醇使用的导入期后,收集诱导痰。包括年龄匹配的非哮喘对照组,以测量年龄相关的炎症变化。与年轻(平均年龄30.8±5.9岁,n= 37)哮喘患者相比,老年(平均年龄67.9± 5.1岁,n = 35)哮喘患者的哮喘控制明显较差,一秒用力呼气量(FEV 1)较低。老年哮喘患者痰中性粒细胞数和百分比(30.5 ×104/mL和23.1%)和嗜酸性粒细胞(7.0×104/mL和3.8%)高于年轻患者(中性粒细胞,13.0 ×104/mL [P<0.01]和6.9% [P<0.01];嗜酸性粒细胞,2.0×104/mL [P <0.01]和1.2% [P<0.01])。老年哮喘患者痰中IL-6(P <0.01)、IL-8(P =0.01)水平明显高于正常对照组。老年人和年轻人对照组之间没有观察到显着的炎症差异。在老年哮喘患者中,痰IL-6和MIP 3 α/CCL 20升高与哮喘控制下降显著相关;痰中性粒细胞、IL-1β、IL-6和MIP 3 α/CCL 20升高与住院时间显著相关。与年轻哮喘患者相比,老年哮喘患者的炎症模式与痰中性粒细胞和嗜酸性粒细胞以及与中性粒细胞募集相关的细胞因子增加有关。气道炎症的差异可能导致老年人哮喘控制能力下降。需要进一步了解老年患者的哮喘病理生理学,以改善这一弱势群体的管理。与年轻哮喘患者相比,老年哮喘患者痰中中性粒细胞和嗜酸性粒细胞以及与中性粒细胞募集相关的细胞因子增加。这些气道炎症的差异与老年人哮喘控制能力下降有关。
Aged asthma patients experience increased morbidity and mortality. Knowledge of the aging effect on airway inflammation and asthma control is limited. To compare airway inflammation and its relationship with asthma control in aged vs. younger patients and determine if differences are asthma-specific or due to “inflamm-aging.” Prospective study of aged (>60 years) and younger (21–40 years) inner-city asthma patients. After a run-in period to control for inhaled corticosteroid use, induced sputum was collected. Aged-matched, non-asthma controls were included to measure age-related inflammatory changes. Aged (mean age 67.9±5.1 years, n=35) compared to younger (mean age 30.8±5.9 years, n=37) asthma patients had significantly worse asthma control and lower forced expiratory volume in one-second (FEV1). Aged asthma patients had higher sputum neutrophil number and percent (30.5 ×104/mL and 23.1%) and eosinophils (7.0×104/mL and 3.8%) compared to younger patients (neutrophils, 13.0 ×104/mL [P<0.01] and 6.9% [P<0.01]; eosinophils, 2.0×104/mL [P <0.01] and 1.2% [P<0.01]). Aged asthma patients had higher sputum interleukin-6 (IL-6) (P <0.01) and IL-8 (P =0.01). No significant inflammatory differences between aged and younger controls were observed. In aged asthma patients, elevated sputum IL-6 and MIP3α/CCL20 were significantly associated with decreased asthma control; elevated sputum neutrophils, IL-1β, IL-6 and MIP3α/CCL20 with hospitalization. The inflammatory patterns of aged vs. younger asthma patients are associated with increased sputum neutrophils and eosinophils and cytokines related to neutrophil recruitment. Differences in airway inflammation may contribute to diminished asthma control in the aged. Further understanding of asthma pathophysiology in aged patients is needed to improve management of this vulnerable population. Aged compared to younger asthma patients have increased sputum neutrophils and eosinophils and cytokines related to neutrophil recruitment. These differences in airway inflammation were associated with diminished asthma control in the aged.