Mycoplasma pneumoniae induces host-dependent pulmonary inflammation and airway obstruction in mice

被引:60
作者
Fonseca-Aten, M
Ríos, AM
Mejías, A
Chávez-Bueno, S
Katz, K
Gómez, AM
McCracken, GH
Hardy, RD
机构
[1] Univ Texas, SW Med Ctr, Dept Pediat, Dallas, TX 75390 USA
[2] Univ Texas, SW Med Ctr, Dept Internal Med, Dallas, TX 75390 USA
[3] Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX 75390 USA
关键词
Mycoplasma pneumoniae; airway obstruction; asthma; airway hyperresponsiveness; cytokines; chemokines;
D O I
10.1165/rcmb.2004-0197OC
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Respiratory tract infections result in wheezing in a subset of patients. Mycoplasma pwneumoniae is a common etiologic agent of acute respiratory infection in children and adults that has been associated with wheezing in 20-40% of individuals. The current study was undertaken to elucidate the host-dependent pulmonary and immunologic response to M. pneumoniae respiratory infection by studying mice with different immunogenetic backgrounds (BALB/c mice versus C57BL/6 mice). After M. pneumoniae infection, only BALB/c mice developed significant airway obstruction (AO) compared with controls. M. pneumoniae-infected BALB/c mice manifested significantly elevated airway hyperresponsiveness (AHR) compared with C57BL/6 mice 4 and 7 d after inoculation as well as BALB/c control mice. Compared with C57BL/6 mice, BALB/c mice developed worse pulmonary inflammation, including greater peribronchial infiltrates. Infected BALB/c mice had significantly higher concentrations of tumor necrosis factor-alpha, interferon-gamma, interleukin (IL)-1beta, IL-6, IL-12, KC (functional IL-8), and macrophage inflammatory protein 1alpha in the bronchoalveolar lavage fluid compared with infected C57BL/6 mice. No differences in IL-2, IL-4, IL-5, IL-10, and granulocyte/macrophage colony-stimulating factor concentrations were found. The mice in this study exhibited host-dependent infection-related AO and AHR associated with chemokine and T-helper type (Th) 1 pulmonary host response and not Th2 response after M. pneumoniae infection.
引用
收藏
页码:201 / 210
页数:10
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