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Commentary

The dichotomy of inhibiting nuclear factor kappa-B in pneumonia

Edward Abraham

Author Affiliations

Office of the Dean, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA

Critical Care 2013, 17:152  doi:10.1186/cc12722


See related research by Devaney et al., http://ccforum.com/content/17/2/R82

Published: 11 June 2013

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.