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Mycoplasma pneumoniae CARDS toxin elicits a functional IgE response in Balb/c mice
Jorge L Medina1, Edward G Brooks1,2, Adriana Chaparro2
1Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
Abstract:
Mycoplasma pneumoniae is strongly associated with new onset asthma and asthma exacerbations. Until recently, the molecular mechanisms utilized by M. pneumoniae to influence asthma symptoms were unknown. However, we recently reported that an ADP-ribosylating and vacuolating toxin called the Community Acquired Respiratory Distress Syndrome toxin, CARDS toxin, produced by M. pneumoniae was sufficient to promote allergic inflammation and asthma-like disease in mice. A mouse model of CARDS toxin exposure was used to evaluate total and CARDS-toxin specific serum IgE responses. Mast cell sensitization, challenge, and degranulation studies determined functionality of the CARDS toxin-specific IgE. In the current study, we report that a single mucosal exposure to CARDS toxin was sufficient to increase total serum IgE and CARDS toxin-specific IgE in mice. Mice given a second mucosal challenge of CARDS toxin responded with significant increases in total and CARDS toxin-specific IgE. CARDS toxin-specific IgE bound to an N-terminal peptide of CARDS toxin but not the C-terminal peptide. Likewise, full-length CARDS toxin and the N-terminal peptide induced mast cell degranulation. Altogether, these data demonstrate that exposure to CARDS toxin is sufficient to generate functional IgE in mice. M. pneumoniae and CARDS toxin are strongly associated with asthma exacerbations raising the possibility that the CARDS toxin-specific IgE-mast cell axis contributes to disease pathogenesis.
Insights
Mycoplasma pneumoniae's CARDS toxin triggers allergic asthma responses in mice. This toxin-specific IgE generation and mast cell activation suggest a new pathway for asthma pathogenesis.
Area of Science:
- Immunology
- Microbiology
- Pulmonology
Background:
- Mycoplasma pneumoniae is linked to asthma development and exacerbations.
- The molecular mechanisms by which M. pneumoniae influences asthma were previously unclear.
- Community Acquired Respiratory Distress Syndrome toxin (CARDS toxin) from M. pneumoniae was identified as a key factor in allergic inflammation and asthma-like disease in mice.
Purpose of the Study:
- To investigate the role of CARDS toxin in generating functional IgE responses.
- To determine if CARDS toxin exposure leads to IgE production and mast cell activation.
- To explore the potential contribution of the CARDS toxin-specific IgE-mast cell axis to asthma pathogenesis.
Main Methods:
- A mouse model was used to assess total and CARDS toxin-specific serum IgE responses after mucosal exposure to CARDS toxin.
- Mast cell sensitization, challenge, and degranulation studies were performed.
- Binding assays determined the specificity of CARDS toxin-specific IgE to toxin peptides.
Main Results:
- A single mucosal exposure to CARDS toxin increased total and CARDS toxin-specific IgE in mice.
- A second exposure led to significant further increases in IgE levels.
- CARDS toxin-specific IgE recognized the N-terminal peptide of the toxin and induced mast cell degranulation.
Conclusions:
- CARDS toxin exposure is sufficient to induce functional IgE production in mice.
- The CARDS toxin-specific IgE-mast cell axis is a potential mechanism contributing to M. pneumoniae-associated asthma exacerbations.
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