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Gains in the fight against acid aspiration lung injury

esolution of injury in vivo, induced proliferation of basal airway epithelial cells and reduced release of the inflammatory cytokine IL-6 in the culture system. In addition, LXA4 further prevents acute inflammation by blocking experimental transmigration of neutrophils into the damaged region. Combined, these events promote restoration of the damaged layer of cells without the added injury that can occur from excessive neutrophil and epithelial cell inflammatory responses.

These data demonstrate the importance of the anti-inflammatory function of LXA4 and its receptors (ALX) in the respiratory tract's ability to heal following acid-aspiration-induced lung injury. The capacity to enhance LXA4 signaling therapeutically may allow faster resolution of such lung injury in patients with severe disease, providing a potential new treatment in the struggle against acid-induced lung diseases, including ARDS.

Finally, this new model of acid aspiration lung injury accurately imitates in vivo cell death and shedding as well as recovery, thus providing researchers a means of testing new treatment strategies for hastening resolution of acid-induced damage.


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Contact: Audra Cox
acox@asip.org
301-634-7409
American Journal of Pathology
2-May-2006


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