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Cell Signaling Underlying The Pathophysiology Of Pneumonia
Sponsored by the APS Respiration Section
Tues. April 4—3:15-5:15 PM
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| Chaired: |
Jahar Bhattacharya,
Columbia Univ.
Jay Mizgerd, Harvard Sch. of Public Hlth. |
Current research addresses the
burgeoning interest in understanding fundamental alveolo-capillary
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. Till recently,
nothing mush was known about these processes. However, new research has
identified mechanisms by which bacteria or bacterial products in the airway
induce alveolo-capillary crosstalk signaling that leads to inflammatory
consequences. The speakers will address these issues in the context of S.
aureus protein A (Prince, Nat Med. 2004; 10:842-8), cytokine receptors (Mizgerd,
Am J Physiol Lung Cell Mol Physiol. 2004;286:L1302-10), P. aeruginosa
exotoxin (Wiener-Kronish, EMBO J. 2003;22:2959-69), and Ca2+-induced
mechanisms (Bhattacharya, J. Clin. Invest. 2003. 111:691-699). These issues
are at the cutting edge of our understanding of the basic mechanisms
underlying lung inflammation and will be presented for the very first time
as a symposium. Each presentation of 25 min will be followed by 5 min of
discussion. We expect the symposium to be of widespread interest.
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3:15 PM |
TPathogen-host interactions in the lung.
Alice Prince, Columbia Univ.
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3:45 PM |
TBacteria-induced cytokine signaling.
Jay Mizgerd, Harvard Sch. of Public Hlth.
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4:15 PM |
Alveolar effects of bacterial exotoxin.
Jeanine Wiener-Kronish, Univ. of California, San Francisco
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4:45 PM |
Lung inflammatory responses
induced by Ca2+-dependent mechanisms.
Jahar Bhattacharya, Columbia Univ.
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