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.
Highlights
Asthma and allergic diseases remain a significant source of morbidity and mortality in the developed world [1]
Allergic diseases remain a significant source of morbidity and in the case of anaphylaxis, risk of mortality
Infection is a significant source of exacerbation in allergic asthma but the mechanisms underlying pathogen-associated disease worsening are poorly understood
Summary
Asthma and allergic diseases remain a significant source of morbidity and mortality in the developed world [1]. This is largely due to the complex interactions between the factors responsible for the etiology of asthma and allergic diseases [2]. Amongst the many factors contributing to allergic diseases; genetics, environment, the microbiota, and infectious agents have significant roles in pathogenesis [2,3,4]. There is strong clinical evidence that both viral and atypical bacterial agents are associated with worsening asthma, and there is growing experimental evidence that they play a role in the genesis of asthma[5,6,7,8,9,10].
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have