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Published on: August 7, 2017
Deficient immune response to Mycoplasma pneumoniae in childhood asthma
T Prescott Atkinson1, Lynn B Duffy, Donna Pendley
1Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama, USA. patkinson@peds.uab.edu
Abstract:
Prospective studies have suggested that some individuals have a persistent IgM response to Mycoplasma pneumoniae infection with relatively little IgG production over many months. Persistence of the organism in patients with an allergic phenotype might predispose to the development of asthma. This study was designed to analyze the prevalence of M. pneumoniae infection and the immune response to that infection among children with asthma compared with controls. A prospective study was performed in 82 children with physician-diagnosed asthma and 98 nonasthmatic controls over a 5-year period comparing them for evidence of current or prior infection by M. pneumoniae using serology (IgG and IgM), culture, and polymerase chain reaction (PCR), and in vitro cellular responses to M. pneumoniae antigen. Similar numbers of controls (9/98) and asthmatic children (6/82) were PCR(+) for M. pneumoniae at some time during the study. IgM antibody to M. pneumoniae was detected in similar numbers of controls (21/98) and asthmatic children (18/82), but positive IgG antibody titers were detected in significantly more controls (13/98) than asthmatic children (3/82; p = 0.03). Similar numbers from each group were IgM(+) on more than one annual visit (9/98 controls and 7/82 asthmatic children). Antigen-driven proliferation and interferon (IFN) gamma production by mononuclear cells from IgM(+) controls were significantly greater than that of IgM(-) controls, but there was no difference in proliferation and IFN-gamma production by cells from IgM(+) and IgM(-) asthmatic children. These results suggest that asthmatic children have deficient cellular and humoral responses to M. pneumoniae infection compared with nonasthmatic controls.
Insights
Asthmatic children show weaker immune responses to Mycoplasma pneumoniae infections compared to healthy children. This suggests impaired cellular and antibody (IgG) production may link Mycoplasma pneumoniae to asthma development.
Area of Science:
- Pediatric Allergy and Immunology
- Infectious Diseases
- Respiratory Medicine
Background:
- Persistent IgM responses to Mycoplasma pneumoniae, with limited IgG, have been observed in some individuals.
- Mycoplasma pneumoniae persistence in allergic individuals may contribute to asthma development.
- Understanding the immune response to Mycoplasma pneumoniae in asthma is crucial for pediatric respiratory health.
Purpose of the Study:
- To investigate the prevalence of Mycoplasma pneumoniae infection and associated immune responses in children with asthma.
- To compare the immune profiles of asthmatic children with Mycoplasma pneumoniae infection against non-asthmatic controls.
- To explore the relationship between Mycoplasma pneumoniae infection and the development or exacerbation of asthma in children.
Main Methods:
- A 5-year prospective study involving 82 children with asthma and 98 non-asthmatic controls.
- Detection of Mycoplasma pneumoniae using serology (IgG, IgM), culture, and polymerase chain reaction (PCR).
- Assessment of in vitro cellular immune responses, including mononuclear cell proliferation and interferon-gamma production.
Main Results:
- Similar PCR positivity for Mycoplasma pneumoniae was found in both asthmatic children and controls.
- Asthmatic children had significantly lower positive IgG antibody titers compared to controls (p = 0.03).
- Mononuclear cells from IgM-positive asthmatic children showed no enhanced proliferation or IFN-gamma production, unlike controls.
Conclusions:
- Asthmatic children exhibit deficient cellular and humoral immune responses to Mycoplasma pneumoniae infection.
- Impaired immune responses may indicate a role for Mycoplasma pneumoniae in asthma pathogenesis.
- Further research is needed to elucidate the specific mechanisms linking Mycoplasma pneumoniae infection and asthma.
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