Abstract

Abstract Mycoplasma pneumoniae is a common human respiratory pathogen that causes acute and chronic respiratory infections that can result in a variety of pulmonary and extra-pulmonary pathologies. M. pneumoniae is associated with exacerbations of human asthma and has significant impact on pathology through unclear mechanisms. We recently demonstrated that Community Acquired Respiratory Distress Syndrome (CARDS) toxin induces an allergic asthma-like disease in naïve mice, as evidenced by a Th2 response, mucus metaplasia and airway hyperreactivity. In this study we examined CARDS toxin’s effects on preexisting asthma using an ovalbumin mouse model of asthma. We show that CARDS toxin can exacerbate pathologies associated with ovalbumin-induced asthma in BALB/c mice both histologically and physiologically. These results were highlighted by increased collagen deposition, shown by picrosirius red staining around medium airways and an increase in eosinophils in the alveolar spaces, shown by cellular differentials. Additionally, these findings are paralleled by heightened Th2 cytokine and chemokine responses as measured by qPCR or ELISA. Finally, lung function assessment via a Flexivent system revealed increases in airway hyperreactivity demonstrated by increased resistance and decreased compliance. The data demonstrate CARDS toxin as a causal factor in the exacerbation of experimental allergic asthma and implicates CARDS toxin as a mediator of morbidity in human asthma.

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