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EB2006 SYMPOSIUM REPORT

Cell signaling underlying the pathophysiology of pneumonia

¹Department of Pediatrics and Pharmacology, Columbia University, New York, New York; ²Harvard School of Public Health, Boston, Massachusetts; ³Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, California; and ⁴Lung Biology Laboratory, Columbia University & St. Luke's-Roosevelt Hospital Center, New York, New York

ABSTRACT

The symposium addressed the burgeoning interest in fundamental mechanisms underlying the onset of pneumonia. Bacteria exploit the lung's innate immune mechanism, resulting in pathophysiological cell signaling. As a consequence inflammation develops, leading to pneumonia. New mechanisms have been identified by which bacteria or bacterial products in the airway induce cross-compartmental signaling that leads to inflammatory consequences. The speakers addressed activation of the transcription factor, NF-B occurring as a consequence of bacterial interactions with specific receptors, such as the Toll-like receptors and the TNF receptor 1 (Prince), or as a consequence of cytokine induction (Mizgerd). Also considered were mechanisms of bacterial virulence in the clinical setting (Wiener-Kronish) and the role of alveolar-capillary signaling mechanisms in the initiation of lung inflammation.

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