title: Cell signaling underlying the pathophysiology of pneumonia.
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-kappaB 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.
authors.affiliation: Department of Pediatrics and Pharmacology, Columbia University, New York, New York, USA.
authors.forename: Alice S
authors.initials: AS
authors.lastname: Prince
authors.forename: Joseph P
authors.initials: JP
authors.lastname: Mizgerd
authors.forename: Jeanine
authors.initials: J
authors.lastname: Wiener-Kronish
authors.forename: Jahar
authors.initials: J
authors.lastname: Bhattacharya
mesh_terms: D002450:Cell Communication; D016207:Cytokines / Q000378:metabolism*; D004848:Epithelium / Q000378:metabolism; D006790:Host-Parasite Interactions; D006801:Humans; D008954:Models, Biological; D011014:Pneumonia / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D011552:Pseudomonas Infections / Q000235:genetics; D011550:Pseudomonas aeruginosa / Q000235:genetics; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000382:microbiology*; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha