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Visualizing Asthma-Causing Immune Cells At Work

ScienceDaily (Nov. 6, 2008) — Immune cells known as eosinophils have a central role in causing asthma. Now, a team of researchers at Massachusetts General Hospital, Boston, has developed approaches to noninvasively visualize in real-time eosinophil responses in the lungs and airways of mice with a disease that mimics asthma (experimental allergic airway inflammation); they hope that these approaches might be developed to help assess the efficacy of treatments (both old and new) for the disease.

The team, led by Mikael Pittet and Ralph Weissleder, visualized eosinophils at single-cell resolution using various noninvasive real-time molecular imaging technologies (specifically, near-infrared fluorescence fiber optic bronchoscopy, intravital microscopy, and fluorescence-mediated tomography) following injection of an optical sensor that targets proteins produced by eosinophils known as MMPs.

Using a combination of the sensitive optical sensor and fluorescence-mediated tomography, it was observed that dexamethasone (a drug used to treat severe asthma) decreased the number of eosinophils in the lungs of mice with allergic airway inflammation.

As some of the imaging techniques have the potential to be developed for the clinic, the authors suggest that in combination with an appropriate optical sensor they might improve our ability to diagnose asthma and assess treatment efficacy.

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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Real-time assessment of inflammation and treatment response in a mouse model of allergic airway inflammation. Journal of Clinical Investigation, (in press)
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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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