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Young male C57BL\/6 mice (25 g) developed ALI following airway deposition of bacterial LPS or IgG immune complexes in the absence or presence of appropriate stereoisomers (enantiomers) of \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    AR agonists, albuterol or formoterol. Endpoints included albumin leak into lung and buildup of polymorphonuclear neutrophils and cytokines\/chemokines in bronchoalveolar fluids. Both \u03b22AR agonists suppressed lung inflammatory parameters (IC\n                    <jats:sub>50<\/jats:sub>\n                    =10\n                    <jats:sup>\u20107<\/jats:sup>\n                    M). Similar effects of \u03b22AR agonists on mediator release were found when mouse macrophages were stimulated\n                    <jats:italic>in vitro<\/jats:italic>\n                    with LPS. The protective effects were associated with reduced activation (phosphorylation) of JNK but not of other signaling proteins. Collectively, these data suggest that \u03b22AR agonists have broad anti\u2010inflammatory effects in the setting of ALI. While \u03b22AR agonists suppress JNK activation, the extent to which this can explain the blunted lung inflammatory responses in the ALI models remains to be determined.\u2014Bosmann, M., Grailer, J. J., Zhu, K., Matthay, M A., Vidya Sarma, J., Zetoune, F. S., Ward, P. A. 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