Dr. Summer's lab publishes key findings regarding acute lung injury

Shah D, Romero F, Stafstrom W, Duong M, Summer R.
Extracellular ATP mediates the late phase of neutrophil recruitment to
the lung in murine models of acute lung injury. Am J Physiol Lung Cell Mol Physiol  2014;306: L152–L161, 2014  

Acute lung injury (ALI) is a severe inflammatory condition whose pathogenesis is irrevocably linked to neutrophil emigration to the lung. Activation and recruitment
of neutrophils to the lung is mostly attributable to local production of
the chemokines. However, much of our understanding of neutrophil
recruitment to the lung is based on studies focusing on early time
points after initiation of injury. In this study, we sought to evaluate the
extended temporal relationship between neutrophil chemotactic factor
expression and influx of neutrophils into the lung after intratracheal
administration of either LPS or bleomycin. In both models, results
demonstrated two phases of neutrophil chemotactic factor expression;
first, an early phase characterized by high levels of CXCL1/keratinocyte-
derived chemokine, CXCL2/monocyte-inhibitory protein-2,
and CXCL5/LPS-induced chemokine expression, and second, a late
phase distinguished by increases in extracellular ATP. Furthermore,
we show that strategies aimed at either enhancing ATP catabolism or inhibiting glycolytic ATP production or reduce extracellular ATP
accumulation, limit vascular leakage, and effectively block the late,
but not the early, stages of neutrophil recruitment to the lung after LPS
instillation. In conclusion, this study illustrates that neutrophil recruitment
to the lung is mediated by the time-dependent expression of
chemotactic factors and suggests that novel strategies, which reduce
extracellular ATP accumulation, may attenuate late neutrophil recruitment
and limit lung injury during ALI.
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