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白细胞介素-4非依赖性途径在支原体呼吸道疾病期间加剧了乙酰甲胆碱诱导的气道高反应性。

IL-4-independent pathways exacerbate methacholine-induced airway hyperreactivity during mycoplasma respiratory disease.

作者信息

Woolard Matthew D, Hardy R Doug, Simecka Jerry W

机构信息

Department of Molecular Biology and Immunology, University of North Texas Health Science, Center, Fort Worth, TX 76107, USA.

出版信息

J Allergy Clin Immunol. 2004 Sep;114(3):645-9. doi: 10.1016/j.jaci.2004.06.019.

Abstract

BACKGROUND

Mycoplasma respiratory infections are associated with wheezing and exacerbation of airway hyperresponsiveness (AHR) in asthmatic patients. IL-4 is a key cytokine in the development of AHR and airway reconstruction in asthmatic patients and might be an important component in exacerbation of AHR during pulmonary mycoplasma infection.

OBJECTIVE

This study evaluates the effect of IL-4 on the severity of methacholine-induced AHR associated with mycoplasma pulmonary mycoplasma infection.

METHODS

BALB/c and IL-4 knockout (KO) mice were infected with Mycoplasma pulmonis, and their enhanced pause scores were monitored before and after methacholine inhalation with whole-body plethysmography.

RESULTS

IL-4 KO mice showed no difference in histopathology of the lungs before or after Mycoplasma pulmonis infection when compared with BALB/c mice. There was an increase in airway obstruction from days 7 to 21 after infection in both strains of mice, but there was no strain difference in airway resistance-associated mycoplasma disease. However, IL-4 KO mice had significantly higher methacholine-induced AHR after M pulmonis infection when compared with BALB/c mice. There was no difference in AHR between uninfected IL-4 KO and control mice.

CONCLUSION

In contrast to our hypothesis, IL-4-independent pathways exacerbate methacholine-induced AHR and promote airway obstruction during the pathogenesis of mycoplasma respiratory disease.

摘要

背景

支原体呼吸道感染与哮喘患者的喘息及气道高反应性(AHR)加重有关。白细胞介素-4(IL-4)是哮喘患者AHR发展和气道重塑过程中的关键细胞因子,可能是肺部支原体感染期间AHR加重的重要组成部分。

目的

本研究评估IL-4对支原体肺部感染相关的乙酰甲胆碱诱导的AHR严重程度的影响。

方法

用肺支原体感染BALB/c和IL-4基因敲除(KO)小鼠,通过全身容积描记法监测乙酰甲胆碱吸入前后它们的增强暂停分数。

结果

与BALB/c小鼠相比,肺支原体感染前后,IL-4 KO小鼠肺部的组织病理学无差异。两种品系小鼠在感染后第7天至第21天气道阻塞均增加,但与支原体疾病相关的气道阻力无品系差异。然而,与BALB/c小鼠相比,肺支原体感染后,IL-4 KO小鼠乙酰甲胆碱诱导的AHR显著更高。未感染的IL-4 KO小鼠和对照小鼠的AHR无差异。

结论

与我们的假设相反,在支原体呼吸道疾病发病机制中,不依赖IL-4的途径会加重乙酰甲胆碱诱导的AHR并促进气道阻塞。

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