The development of asthma in children infected with Chlamydia pneumoniae is dependent on the modifying effect of mannose-binding lectin
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Published on: April 16, 2019
Adrienne Nagy1, Gergely T Kozma, Márton Keszei
1Budai Children's Hospital, Budapest, Hungary.
Insights
Variant mannose-binding lectin (MBL) alleles increase children's asthma risk when infected with Chlamydia pneumoniae. Chronic infections with variant MBL alleles significantly heighten this risk, suggesting a key role in asthma development.
Area of Science:
- Pediatric Allergy and Immunology
- Infectious Diseases
- Genetics
Background:
- Chlamydia pneumoniae infections are linked to asthma exacerbations in adults, but its role in childhood asthma initiation is unclear.
- Previous research on C. pneumoniae and childhood asthma development yielded controversial results.
Purpose of the Study:
- To investigate the role of C. pneumoniae infection in childhood asthma.
- To examine how mannose-binding lectin (MBL) variant alleles modify asthma susceptibility in children with C. pneumoniae infection.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) for C. pneumoniae-specific antibodies.
- Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) for MBL genotyping.
Main Results:
- No overall difference in C. pneumoniae antibodies between asthmatic children and controls.
- Asthmatic children with variant MBL alleles showed higher C. pneumoniae IgG levels (63.7% vs 40.7%).
- Variant MBL alleles increased asthma risk in infected children, particularly with chronic/recurrent infections (OR 5.38).
Conclusions:
- Variant MBL alleles are crucial for asthma susceptibility in children with C. pneumoniae infection.
- This genetic factor significantly influences the development of asthma following C. pneumoniae exposure.
Background:
Although several studies found associations between infection with Chlamydia pneumoniae and asthma, these were mainly restricted to the exacerbation of the symptoms in adults with known asthma. Data about the role of C pneumoniae in the initiation and development of asthma in children are controversial.
Objective:
We investigated the role of C pneumoniae infection in 139 children with asthma, comparing them with 174 healthy control subjects. Furthermore, we studied the modifying effect of mannose-binding lectin (MBL) variant alleles on the susceptibility to asthma in children infected with C pneumoniae.
Methods:
C pneumoniae-specific antibodies were measured by means of ELISA, and MBL genotypes were determined by means of PCR-RFLP.
Results:
There were no significant differences in the percentage of children with positive results for C pneumoniae-specific antibodies between patients and control subjects. Among asthmatic children carrying variant MBL alleles, there were significantly more patients with positive results for C pneumoniae-specific IgG than among control children with variant MBL genotypes (63.7% vs 40.7% of asthmatic vs control children, respectively; odds ratio adjusted for age and sex, 2.21; 95% CI, 1.10-4.41; P =.02). Infected children with variant MBL alleles were found to have a higher risk of asthma development than infected children with normal MBL genotype. This risk was especially high in children with chronic or recurrent infection (positive results for both IgA and IgG; adjusted odds ratio, 5.38; 95% CI, 1.75-14.36; P =.01), but no increased risk was seen in children with current C pneumoniae infection (positive results for IgM).
Conclusion:
This study indicates the important role of variant MBL alleles in the susceptibility to asthma in children infected with C pneumoniae.
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