Bronchial asthma is exacerbated by Mycoplasma pneumoniae–induced upper respiratory tract infections (URTIs) 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.
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 6 months.
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 nonasthmatic controls (N = 23 and 13, respectively) (UniCAP total IgE Fluoroenzymeimmunoassay, enzyme-linked immunosorbent assay).
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 nonasthmatics (median [interquartile range]: 0.57 [1.00] versus 0.21 [0.19]; Kruskal–Wallis test, P = 0.0008). In addition, IgM positivity was significantly higher in asthmatic compared with nonasthmatic subjects (39.1% versus 0.0%; Fisher’s 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).
Increased specific IgM anti–M. pneumoniae responses may indicate an important role for M. pneumoniae infection in asthma.
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From the *Department of Pediatrics, Center for Allergy and Asthma Research, SUNY Downstate Medical Center, Brooklyn, NY; †Department of Dermatology, St. Luke’s-Roosevelt Hospital and Beth Israel Medical Centers, New York, NY; Departments of ‡Medicine and §Pathology, Center for Allergy and Asthma Research, SUNY Downstate Medical Center, Brooklyn, NY; and ¶Department of Pathology, Wayne State University School of Medicine, Detroit, MI.
Accepted for publication January 04, 2013.
This work has been funded by a NY State Divisional Grant. The authors have no other funding or conflicts of interest to disclose.
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Address for correspondence: Tamar A. Smith-Norowitz, PhD, Associate Professor, Department of Pediatrics, SUNY Downstate Medical Center, Box 49, 450 Clarkson Ave., Brooklyn, New York 11203. E-mail: firstname.lastname@example.org.