哮喘联盟

   摘要
   背景：在儿童中，肺炎支原体导致的上呼吸道感染（URTI）常可使支气管哮喘加重。特异性IgM和IgG参与了肺炎支原体的免疫应答过程，但对肺炎支原体特异性IgE在哮喘中的作用却了解甚少。
   目的：研究肺炎支原体特异性IgM、IgG和IgE抗体与儿童过去6个月内出现URTI的相关性。
   方法：在肺炎支原体阳性和阴性的稳定期哮喘患儿（n=23；无当前恶化）和非哮喘对照者（n=13）中，检测总抗体和肺炎支原体IgM、IgG和IgE抗体（UniCAP总IgE荧光酶免疫分析, ELISA, 免疫杂交）。
   结果：与非哮喘对照者相比，哮喘患儿中的特异性IgM与特异性IgG相关（Spearman相关分析, rho=0.61, P<0.0001），但与特异性IgE抗肺炎支原体抗体（AMA）无关。然而，特异性IgG浓度与特异性IgE AMA相关（rho=0.49, P=0.0017）。与非哮喘对照者相比，哮喘患儿的特异性IgM AMA水平较高（中位数[四分位间距]：0.57 [1.00] vs. 0.21 [0.19]；Kruskal-Wallis检验：P=0.0008）。此外，哮喘患儿中的IgM阳性率高于非哮喘对照者（39.1% vs. 0.0%; Fisher 精确检验, P=0.01）。上述结果独立于过去6个月的URTI病史，后者也与较高的IgM、IgG和IgE AMA水平无关（P=0.25-0.64）。
   结论：特异性IgM 抗肺炎支原体反应在哮喘患儿肺炎支原体感染中具有重要作用。
 

（刘国梁 审校）
Pediatr Infect Dis J. 2013 Jan 23. [Epub ahead of print]

 

Asthmatic Children have Increased Specific Anti-Mycoplasma pneumoniae IgM but not IgG or IgE- Values Independent of History of Respiratory Tract Infection.
 
Smith-Norowitz TA, Silverberg JI, Kusonruksa M, Weaver D, Ginsburg D, Norowitz KB, Durkin HG,Hammerschlag MR, Bluth MH, Kohlhoff SA.

Source
Departments of Pediatrics, 1, Medicine, 3, and Pathology, 4, *Center for Allergy and Asthma Research, S.U.N.Y. Downstate Medical Center, Brooklyn, New York 11203, Department of Dermatology, 2, St. Luke's-Roosevelt Hospital and Beth Israel Medical Centers, New York, NY 10025, USA, Department of Pathology, 5, Wayne State University School of Medicine, Detroit, Michigan, 48201.

Abstract 
BACKGROUND: Bronchial asthma is exacerbated by Mycoplasma pneumoniae -induced upper respiratory tract infections (URTI) in children. Specific IgM and IgG isotypes are involved in the immune response to M. pneumoniae, but little is known about the role of specific IgE antibodies against M. pneumoniae in asthma.
OBJECTIVE:To investigate the role of IgM, IgG, and IgE specific antibody responses to M. pneumoniae in children with persistent asthma in relationship to history of URTI within the past six months.
METHODS:Total or specific anti-M. pneumoniae IgM, IgG and IgE antibody responses were studied in stable asthmatic pediatric patients (M. pneumoniae positive and negative) without current exacerbation and non-asthmatic controls (N=23, and 13, respectively). (UniCAP total IgE Fluoroenzyme immunoassay, ELISA, Immunoblot).
RESULTS: Values of specific IgM correlated with specific IgG (Spearman correlation, rho=0.61, P<0.0001) but not with specific IgE anti M. pneumoniae antibodies (AMA) in asthmatic subjects compared with nonasthmatic controls. However, concentrations of specific IgG correlated with specific IgE AMA (rho=0.49, P=0.0017). Asthmatic subjects had higher levels of specific IgM AMA levels compared with non-asthmatics (median [interquartile range]: 0.57 [1.00] vs. 0.21 [0.19]; Kruskal-Wallis test, P=0.0008). In addition, IgM positivity was significantly higher in asthmatic compared with non-asthmatic subjects (39.1% vs. 0.0%; Fisher exact test, P=0.01). These results were independent of URTI history in the past 6 months, which was not associated with higher IgM, IgG or IgE AMA levels compared with no URTI history (P=0.25-0.64).
CONCLUSIONS: Increased specific IgM anti-M. pneumoniae responses may indicate an important role for M. pneumoniae infection in asthma.
 

Pediatr Infect Dis J. 2013 Jan 23. [Epub ahead of print]