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Journal of Endotoxin Research
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Pulmonary TNF{alpha} is a critical mediator in Adult Respiratory Distress Syndrome

G.Z. Feuerstein

Department of Cardiovascular Pharmacology, SmithKline Beecham, King of Prussia, Department of Surgery, Jefferson Medical College, Philadelphia, Pennsylvania, USA

L.F. Neville

Department of Cardiovascular Pharmacology, SmithKline Beecham, King of Prussia, Department of Surgery, Jefferson Medical College, Philadelphia, Pennsylvania, USA

R. Rabinovici

Department of Cardiovascular Pharmacology, SmithKline Beecham, King of Prussia, Department of Surgery, Jefferson Medical College, Philadelphia, Pennsylvania, USA

The development of effective pharmacotherapies to combat the Adult Respiratory Distress Syndrome (ARDS) is critically dependent upon: (1) the development of clinically-relevant animal models; (2) identification of inflammatory mediators centrally involved in eliciting lung injury; (3) understanding the inter-relationships or 'cross-talk' between pro and anti-inflammatory mediators which modulate the lung inflammation; and (4) the application of molecular techniques to isolate potentially novel genes involved in the development of ARDS. In this paper, we will present evidence from a rat model of microvascular lung injury produced by interleukin-2 (IL-2), that pulmonary TNF{alpha} is a primary and pivotal mediator of lung injury and that different modes of TNF{alpha} inhibition may represent feasible strategies to prevent ARDS. Furthermore, we will describe how the application of Differential Display Reverse Transcriptase Polymerase Chain Reaction (DDRT-PCR) can allow the rapid isolation of partial fragments of potentially new genes involved in ARDS. The products of such genes could represent future target sites for pharmacotherapeutic intervention.

Journal of Endotoxin Research, Vol. 2, No. 3, 189-193 (1995)
DOI: 10.1177/096805199500200307
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