Mycoplasma pneumoniae CARDS toxin elicits a functional IgE response in Balb/c mice

• Published in: PloS one 2017-02, Vol.12 (2), p.e0172447-e0172447
• Main Authors: Medina, Jorge L, Brooks, Edward G, Chaparro, Adriana, Dube, Peter H
• Format: Article
• Language: English
• Subjects: Allergies; Animals; Asthma; Bacterial Proteins - chemistry; Bacterial Proteins - genetics; Bacterial Proteins - immunology; Bacterial Proteins - metabolism; Bacterial Toxins - chemistry; Bacterial Toxins - genetics; Bacterial Toxins - immunology; Bacterial Toxins - metabolism; Biology and Life Sciences; Bone marrow; Bone Marrow Cells - cytology; Bone Marrow Cells - metabolism; Cards; Cells, Cultured; Degranulation; Disease Models, Animal; Epitopes - immunology; Exposure; Hexosaminidases; Hypersensitivity; Immunoglobulin E; Immunoglobulin E - blood; Immunoglobulins; Immunology; Infections; Infectious diseases; Inflammation; Laboratories; Lupus; Medicine and Health Sciences; Mice; Mice, Inbred BALB C; Molecular modelling; Mucosa; Mycoplasma pneumoniae; Mycoplasma pneumoniae - metabolism; Pathogenesis; Pediatrics; Pneumonia; Recombinant Proteins - biosynthesis; Recombinant Proteins - immunology; Recombinant Proteins - isolation & purification; Research and Analysis Methods; Respiratory distress syndrome; Science; STAT6 Transcription Factor - genetics; STAT6 Transcription Factor - metabolism; Studies; Toxins; Viral infections; Whooping cough
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0172447

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.