title: Mycoplasma pneumoniae CARDS toxin elicits a functional IgE response in Balb/c mice.
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.
authors.affiliation: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Jorge L
authors.initials: JL
authors.lastname: Medina
authors.affiliation: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.|Department of Pediatrics, Division of Immunology and Infectious Diseases, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Edward G
authors.initials: EG
authors.lastname: Brooks
authors.affiliation: Department of Pediatrics, Division of Immunology and Infectious Diseases, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Adriana
authors.initials: A
authors.lastname: Chaparro
authors.affiliation: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Peter H
authors.identifier: http://orcid.org/0000-0002-8755-3737
authors.initials: PH
authors.lastname: Dube
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000737:chemistry / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D001427:Bacterial Toxins / Q000737:chemistry / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D001854:Bone Marrow Cells / Q000166:cytology / Q000378:metabolism; D002478:Cells, Cultured; D004195:Disease Models, Animal; D000939:Epitopes / Q000276:immunology; D006596:Hexosaminidases; D007073:Immunoglobulin E / Q000097:blood*; D051379:Mice; D008807:Mice, Inbred BALB C; D009177:Mycoplasma pneumoniae / Q000378:metabolism*; D011994:Recombinant Proteins / Q000096:biosynthesis / Q000276:immunology / Q000302:isolation & purification; D050800:STAT6 Transcription Factor / Q000235:genetics / Q000378:metabolism
chemical_list: D001426:Bacterial Proteins; D001427:Bacterial Toxins; C546120:CARDS toxin, Mycoplasma pneumoniae; D000939:Epitopes; D011994:Recombinant Proteins; D050800:STAT6 Transcription Factor; D007073:Immunoglobulin E; D006596:Hexosaminidases