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肺炎支原体可引发慢性呼吸道感染、气道高反应性和肺部炎症:一种感染相关性慢性反应性气道疾病的小鼠模型。

Mycoplasma pneumoniae induces chronic respiratory infection, airway hyperreactivity, and pulmonary inflammation: a murine model of infection-associated chronic reactive airway disease.

作者信息

Hardy Robert D, Jafri Hasan S, Olsen Kurt, Hatfield Jeanine, Iglehart Janie, Rogers Beverly B, Patel Padma, Cassell Gail, McCracken George H, Ramilo Octavio

机构信息

Department of Pediatric Infectious Diseases, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

出版信息

Infect Immun. 2002 Feb;70(2):649-54. doi: 10.1128/IAI.70.2.649-654.2002.

Abstract

Because chronic Mycoplasma pneumoniae respiratory infection is hypothesized to play a role in asthma, the potential of M. pneumoniae to establish chronic respiratory infection with associated pulmonary disease was investigated in a murine model. BALB/c mice were intranasally inoculated once with M. pneumoniae and examined at 109, 150, 245, 368, and 530 days postinoculation. M. pneumoniae was detected in bronchoalveolar lavage fluid by culture or PCR in 70 and 22% of mice at 109 and 530 days postinoculation, respectively. Lung histopathology was normal up to 368 days postinoculation. At 530 days, however, 78% of the mice inoculated with M. pneumoniae demonstrated abnormal histopathology characterized by peribronchial and perivascular mononuclear infiltrates. A mean histopathologic score (HPS) at 530 days of 5.1 was significantly greater (P < 0.01) than that for controls (HPS score of 0). Serum anti-M. pneumoniae immunoglobulin G was detectable in all of the mice inoculated with M. pneumoniae and was inversely correlated with HPS (r = -0.95, P = 0.01) at 530 days postinoculation. Unrestrained whole-body plethysmography measurement of enhanced pause revealed significantly elevated airway methacholine reactivity in M. pneumoniae-inoculated mice compared with that in controls at 245 days (P = 0.03) and increased airway obstruction at 530 days (P = 0.01). Murine M. pneumoniae respiratory infection can lead to chronic pulmonary disease characterized by airway hyperreactivity, airway obstruction, and histologic inflammation.

摘要

由于慢性肺炎支原体呼吸道感染被认为在哮喘中起作用,因此在小鼠模型中研究了肺炎支原体引发伴有肺部疾病的慢性呼吸道感染的可能性。将BALB/c小鼠经鼻接种一次肺炎支原体,并在接种后109、150、245、368和530天进行检查。接种后109天和530天,分别有70%和22%的小鼠通过培养或PCR在支气管肺泡灌洗液中检测到肺炎支原体。接种后368天内肺组织病理学均正常。然而,在530天时,78%接种肺炎支原体的小鼠表现出异常的组织病理学特征,以支气管周围和血管周围单核细胞浸润为特点。530天时的平均组织病理学评分(HPS)为5.1,显著高于对照组(HPS评分为0)(P<0.01)。接种肺炎支原体的所有小鼠血清中均可检测到抗肺炎支原体免疫球蛋白G,且在接种后530天时与HPS呈负相关(r=-0.95,P=0.01)。通过无限制全身体积描记法测量增强间歇,发现接种肺炎支原体的小鼠在245天时气道对乙酰甲胆碱的反应性显著高于对照组(P=0.03),在530天时气道阻塞增加(P=0.01)。小鼠肺炎支原体呼吸道感染可导致以气道高反应性、气道阻塞和组织学炎症为特征的慢性肺部疾病。

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