ArticleThe journal of trauma and acute care surgery2015
SIRT1 mediates a primed response to immune challenge after traumatic lung injury.
Article in The journal of trauma and acute care surgery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Xiaoxianxiong Decoction Attenuates LPS-Induced Pneumonia in Mice by Inhibiting Inflammatory Response Through Activation of SIRT1.FASEB bioAdvances · 2025Article
- Citicoline and COVID-19-Related Cognitive and Other Neurologic Complications.Brain sciences · 2021Review
- NADFrontiers in molecular biosciences · 2021Review
- COVID-19: NADMedical hypotheses · 2020Article
- Sirtuins: potential therapeutic targets for regulating acute inflammatory response?Expert opinion on therapeutic targets · 2020Review
- Resveratrol decreases CD45Journal of cellular and molecular medicine · 2019Article
- Switch of NAD Salvage toFrontiers in immunology · 2019Article
- A Study of the Therapeutic Effects of Resveratrol on Blunt Chest Trauma-Induced Acute Lung Injury in Rats and the Potential Role of Endocan as a Biomarker of Inflammation.Inflammation · 2017Article
- Sirtuins Link Inflammation and Metabolism.Journal of immunology research · 2016Review
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundPulmonary contusion (PC) is a common, potentially lethal injury that results in priming for exaggerated inflammatory responses to subsequent immune challenge like infection (second hit). The molecular mechanism of priming and the second hit phenomenon after PC remain obscure. With the use of a mouse model of PC, this study explores the role of sirtuin 1 (SIRT1), an NAD+-dependent deacetylase, in priming for a second hit after injury.
methodsWith the use of a mouse model of PC, injury-primed second-hit host responses were tested at 24 hours after PC by (1) in vivo infectious challenge of injured mice or (2) ex vivo inflammatory challenge of isolated immune cells from injured mice. SIRT activators or repressors were used to test for SIRT1 participation in these second-hit responses.
resultsPC-injured mice given an in vivo infectious challenge by cecal ligation and puncture (CLP) had significantly increased mortality compared with injury or infectious challenge alone. Isolated bronchoalveolar lavage (BAL) cells from injured mice given an ex vivo inflammatory challenge with bacterial lipopolysaccharide (LPS) had increased levels of tumor necrosis factor α messenger RNA compared with uninjured mice. We found that PC reduced SIRT1 protein, messenger RNA, and SIRT1 enzymatic activity in injured lung tissue. We also found decreased SIRT1 protein levels in BAL cells from injured mice. We further found that injured mice treated with a SIRT1 activator, resveratrol, showed significantly decreased polymorphonuclear leukocytes (PMN) in the BAL in response to intratracheal LPS and increased survival from CLP.
conclusionThese results showed that PC decreased SIRT1 levels in the lung correlated with enhanced responses to infectious or inflammatory stimuli in injured mice. Treatment of injured mice with a SIRT1 activator, resveratrol, decreased LPS inflammatory response and increased survival after CLP. Our results suggest that SIRT1 participates in the second-hit response after injury.
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