title: The dichotomy of inhibiting nuclear factor kappa-B in pneumonia.
abstract: Activation of nuclear factor kappa-B (NF-κB) results in its translocation from the cytoplasm to the nucleus and binding to the promoters of a large number of genes, including those encoding proinflammatory cytokines and other mediators that can contribute to organ system dysfunction in severe infection. While inhibition of NF-κB activation has been proposed as a therapeutic approach in critical illness, several studies have indicated that such an approach may have deleterious effects in persistent infectious states, such as pneumonia. A new report from Devaney and colleagues shows that while inhibition of NF-κB may be useful in severe pneumonia associated with rapid progression to mortality, it leads to worsened pulmonary injury with increased bacterial numbers in the lungs in a model of prolonged pneumonia. Such data raise concerns about therapeutic approaches targeting NF-κB in critically ill patients with persistent infection.
authors.forename: Edward
authors.initials: E
authors.lastname: Abraham
mesh_terms: D000818:Animals; D004927:Escherichia coli Infections / Q000188:drug therapy* / Q000473:pathology*; D020672:I-kappa B Proteins / Q000008:administration & dosage*; D008297:Male; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000037:antagonists & inhibitors*; D018410:Pneumonia, Bacterial / Q000188:drug therapy* / Q000473:pathology*; D012720:Severity of Illness Index
chemical_list: D020672:I-kappa B Proteins; D016328:NF-kappa B; D000072000:NF-KappaB Inhibitor alpha