Selected article for: "ARDS pathogenesis and lung inflammation"

Author: Sadikot, Ruxana T.; Kolanjiyil, Arun V.; Kleinstreuer, Clement; Rubinstein, Israel
Title: Nanomedicine for Treatment of Acute Lung Injury and Acute Respiratory Distress Syndrome
  • Document date: 2017_6_27
  • ID: 27gutwjd_6
    Snippet: The molecular pathobiology of ARDS is being extensively defined and the role of several molecules including pattern recognition receptors present on the immune cells (e.g., Toll-like receptors, Nod-like receptors, inflammasomes, and downstream signaling molecules such as NF-κB) and effector molecules (e.g., TNF-α, IL-1β, and IL-18) are being investigated in the pathogenesis of ALI and ARDS. Targeting central molecules such as NF-κB attenuates.....
    Document: The molecular pathobiology of ARDS is being extensively defined and the role of several molecules including pattern recognition receptors present on the immune cells (e.g., Toll-like receptors, Nod-like receptors, inflammasomes, and downstream signaling molecules such as NF-κB) and effector molecules (e.g., TNF-α, IL-1β, and IL-18) are being investigated in the pathogenesis of ALI and ARDS. Targeting central molecules such as NF-κB attenuates lung inflammation but has major limitations because inhibition of NF-κB is immunosuppressive and compromises host defense [22] . However, due to the complex nature of the disease, targeting single cytokines or chemokines has also failed to attenuate lung inflammation as these are not sufficient singly to attenuate lung inflammation in ARDS.

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