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Therapeutics for acute lung injury: time to call in the DRs?

Therapeutics for acute lung injury: time to call in the DRs?
Therapeutics for acute lung injury: time to call in the DRs?
Lung inflammation is a prominent feature of both acute and chronic respiratory syndromes. Classically, in conditions like non-pulmonary sepsis, pneumonia or chronic obstructive lung disease (COPD), this inflammation has been associated with infection, but may also result from other non-infectious insults, such as trauma or injury. Both infectious and non-infectious insults can lead to Acute Lung Injury(ALI)/Acute Respiratory Distress Syndrome (ARDS), where regardless of the underlying stimuli, the net result of the inflammation initiated is damage to the alveolar-capillary membrane which can result in respiratory failure [1]. As the underlying mechanisms unifying these diverse insults are not well understood, the development of new treatments has also lagged behind. Even where we think we understand the initiating stimulus, for example in sepsis, targeting inflammatory pathways with pleiotropic anti-inflammatory drugs such as steroids or aspirin provide little benefit and ALI/ARDS outcomes remain poor. Moreover, even ?2-agonists, which might be thought to provide some benefit due to their bronchodilator action, have not been demonstrated to provide any improvement in clinical outcomes [2]. Thus, there is a pressing need to identify new therapeutic targets to reduce ALI/ARDS morbidity and mortality.
0741-5400
351-353
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee

Staples, Karl J. (2017) Therapeutics for acute lung injury: time to call in the DRs? Journal of Leukocyte Biology, 101 (2), 351-353. (doi:10.1189/jlb.3CE1016-370R). (PMID:28148762)

Record type: Editorial

Abstract

Lung inflammation is a prominent feature of both acute and chronic respiratory syndromes. Classically, in conditions like non-pulmonary sepsis, pneumonia or chronic obstructive lung disease (COPD), this inflammation has been associated with infection, but may also result from other non-infectious insults, such as trauma or injury. Both infectious and non-infectious insults can lead to Acute Lung Injury(ALI)/Acute Respiratory Distress Syndrome (ARDS), where regardless of the underlying stimuli, the net result of the inflammation initiated is damage to the alveolar-capillary membrane which can result in respiratory failure [1]. As the underlying mechanisms unifying these diverse insults are not well understood, the development of new treatments has also lagged behind. Even where we think we understand the initiating stimulus, for example in sepsis, targeting inflammatory pathways with pleiotropic anti-inflammatory drugs such as steroids or aspirin provide little benefit and ALI/ARDS outcomes remain poor. Moreover, even ?2-agonists, which might be thought to provide some benefit due to their bronchodilator action, have not been demonstrated to provide any improvement in clinical outcomes [2]. Thus, there is a pressing need to identify new therapeutic targets to reduce ALI/ARDS morbidity and mortality.

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Accepted/In Press date: 8 November 2016
e-pub ahead of print date: 1 February 2017
Organisations: Clinical & Experimental Sciences

Identifiers

Local EPrints ID: 402461
URI: https://eprints.soton.ac.uk/id/eprint/402461
ISSN: 0741-5400
PURE UUID: f6b3297f-c859-4ccc-a4d6-3d85f6422c8f
ORCID for Karl J. Staples: ORCID iD orcid.org/0000-0003-3844-6457

Catalogue record

Date deposited: 09 Nov 2016 11:30
Last modified: 10 Aug 2019 00:34

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