Mycoplasma pneumoniae CARDS Toxin Exacerbates Ovalbumin-Induced Asthma-Like Inflammation in BALB/c Mice.

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Mycoplasma pneumoniae CARDS Toxin Exacerbates Ovalbumin-Induced Asthma-Like Inflammation in BALB/c Mice.

PLoS One. 2014;9(7):e102613

Authors: Medina JL, Coalson JJ, Brooks EG, Le Saux CJ, Winter VT, Chaparro A, Principe MF, Solis L, Kannan TR, Baseman JB, Dube PH

Abstract
Mycoplasma pneumoniae causes a range of airway and extrapulmonary pathologies in humans. Clinically, M. pneumoniae is associated with acute exacerbations of human asthma and a worsening of experimentally induced asthma in mice. Recently, we demonstrated that Community Acquired Respiratory Distress Syndrome (CARDS) toxin, an ADP-ribosylating and vacuolating toxin synthesized by M. pneumoniae, is sufficient to induce an asthma-like disease in BALB/cJ mice. To test the potential of CARDS toxin to exacerbate preexisting asthma, we examined inflammatory responses to recombinant CARDS toxin in an ovalbumin (OVA) murine model of asthma. Differences in pulmonary inflammatory responses between treatment groups were analyzed by histology, cell differentials and changes in cytokine and chemokine concentrations. Additionally, assessments of airway hyperreactivity were evaluated through direct pulmonary function measurements. Analysis of histology revealed exaggerated cellular inflammation with a strong eosinophilic component in the CARDS toxin-treated group. Heightened T-helper type-2 inflammatory responses were evidenced by increased expression of IL-4, IL-13, CCL17 and CCL22 corresponding with increased airway hyperreactivity in the CARDS toxin-treated mice. These data demonstrate that CARDS toxin can be a causal factor in the worsening of experimental allergic asthma, highlighting the potential importance of CARDS toxin in the etiology and exacerbation of human asthma.

PMID: 25058417 [PubMed – in process]

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Predictive value of C-reactive protein in response to macrolides in children with macrolide-resistant Mycoplasma pneumoniae pneumonia.

Predictive value of C-reactive protein in response to macrolides in children with macrolide-resistant Mycoplasma pneumoniae pneumonia.

Korean J Pediatr. 2014 Apr;57(4):186-92

Authors: Seo YH, Kim JS, Seo SC, Seo WH, Yoo Y, Song DJ, Choung JT

Abstract
PURPOSE: The prevalence of macrolide-resistant Mycoplasma pneumoniae (MRMP) has increased worldwide. The aim of this study was to estimate the proportion of MRMP in a tertiary hospital in Korea, and to find potential laboratory markers that could be used to predict the efficacy of macrolides in children with MRMP pneumonia.
METHODS: A total of 95 patients with M. pneumoniae pneumonia were enrolled in this study. Detection of MRMP was based on the results of specific point mutations in domain V of the 23S rRNA gene. The medical records of these patients were reviewed retrospectively and the clinical course and laboratory data were compared.
RESULTS: The proportion of patients with MRMP was 51.6% and all MRMP isolates had the A2063G point mutation. The MRMP group had longer hospital stay and febrile period after initiation of macrolides. The levels of serum C-reactive protein (CRP) and interleukin-18 in nasopharyngeal aspirate were significantly higher in patients who did not respond to macrolide treatment. CRP was the only significant factor in predicting the efficacy of macrolides in patients with MRMP pneumonia. The area under the curve for CRP was 0.69 in receiver operating characteristic curve analysis, indicating reasonable discriminative power, and the optimal cutoff value was 40.7 mg/L.
CONCLUSION: The proportion of patients with MRMP was high, suggesting that the prevalence of MRMP is rising rapidly in Korea. Serum CRP could be a useful marker for predicting the efficacy of macrolides and helping clinicians make better clinical decisions in children with MRMP pneumonia.

PMID: 24868216 [PubMed]

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