Evidence map›Paper›PMID 20200273›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Febrile-range hyperthermia augments lipopolysaccharide-induced lung injury by a mechanism of enhanced alveolar epithelial apoptosis.

Anne B Lipke, Gustavo Matute-Bello, Raquel Herrero, Kiyoyasu Kurahashi, Venus A Wong, Stephen M Mongovin, Thomas R Martin

2 registry-linked trialsOpen access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT03376854 phase2withdrawnnot on this mapstarted 2018, after this paper: background citation

Pilot Randomized Clinical Trial of Therapeutic Hypothermia Plus Neuromuscular Blockade vs. Standard of Care in COVID-19 Patients With Moderate to Severe ARDS - the Cooling to Help Injured Lungs (CHILL) Pilot Study

TypeinterventionalSponsorUniversity of Maryland, BaltimoreRan2018 to 2021Enrolled0ConditionsRespiratory Distress Syndrome, Adult, Sars-CoV2ArmsHypothermia, Neuromuscular Blocking Agents, Standard of Care
NCT04545424 phase2recruitingnot on this mapstarted 2021, after this paper: background citation

Cooling to Help Injured Lungs (CHILL) Phase IIB Randomized Control Trial of Therapeutic Hypothermia in Patients With ARDS

TypeinterventionalSponsorUniversity of Maryland, BaltimoreRan2021 to 2026Enrolled340ConditionsRespiratory Distress Syndrome, AdultArmsHypothermia, Neuromuscular Blocking Agents, Standard of care
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Body temperature and mortality in patients with acute respiratory distress syndrome.American journal of critical care : an official publication, American Association of Critical-Care Nurses · 2015
    Trial
  2. Article
  3. Article
  4. Article
  5. Temperature control in sepsis.Frontiers in medicine · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  12. Exposure to febrile-range hyperthermia potentiates Wnt signalling and epithelial-mesenchymal transition gene expression in lung epithelium.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2018
    Article
  13. Review
  14. Activation of heat shock response augments fibroblast growth factor-1 expression in wounded lung epithelium.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Hyperthermia promotes and prevents respiratory epithelial apoptosis through distinct mechanisms.American journal of respiratory cell and molecular biology · 2012
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Anne B LipkeMedical Research Service, VA Puget Sound Medical Center, University of Washington, Seattle, WA 98108, USA.
Gustavo Matute-Bello
Raquel Herrero
Kiyoyasu Kurahashi
Venus A Wong
Stephen M Mongovin
Thomas R Martin
University of Puget Sound · USUniversity of Washington · USYokohama City University · JP

Funding

The alveolar epithelium in lung injury and repairR01HL083044 · NHLBI · UNIVERSITY OF WASHINGTON · PI MATUTE-BELLO, GUSTAVO · 2006 to 2010
$2.3M
Acute Lung Injury: Link Between Apoptosis and Fibrosis R01HL081764 · NHLBI · UNIVERSITY OF WASHINGTON · PI MATUTE-BELLO, GUSTAVO · 2007 to 2011
$1.6M
Mechanisms of enhanced lung epithelial injury in febrile hyperthermiaF32HL096348 · NHLBI · UNIVERSITY OF WASHINGTON · PI LIPKE, ANNE B · 2009 to 2010
$119k
NHLBI NIH HHS F32 HL096348NHLBI NIH HHS HL081764NHLBI NIH HHS HL083044NHLBI NIH HHS HL096348NHLBI NIH HHS R01 HL081764NHLBI NIH HHS R01 HL083044
6 · The paper itself

Abstract

Fever is common in critically ill patients and is associated with worse clinical outcomes, including increased intensive care unit mortality. In animal models, febrile-range hyperthermia (FRH) worsens acute lung injury, but the mechanisms by which this occurs remain uncertain. We hypothesized that FRH augments the response of the alveolar epithelium to TNF-alpha receptor family signaling. We found that FRH augmented LPS-induced lung injury and increased LPS-induced mortality in mice. At 24 h, animals exposed to hyperthermia and LPS had significant increases in alveolar permeability without changes in inflammatory cells in bronchoalveolar lavage fluid or lung tissue as compared with animals exposed to LPS alone. The increase in alveolar permeability was associated with an increase in alveolar epithelial apoptosis and was attenuated by caspase inhibition with zVAD.fmk. At 48 h, the animals exposed to hyperthermia and LPS had an enhanced lung inflammatory response. In murine lung epithelial cell lines (MLE-15, LA-4) and in primary type II alveolar epithelial cells, FRH enhanced apoptosis in response to TNF-alpha but not Fas ligand. The increase in apoptosis was caspase-8 dependent and associated with suppression of NF-kappaB activity. The FRH-associated NF-kappaB suppression was not associated with persistence of IkappaB-alpha, suggesting that FRH-mediated suppression of NF-kappaB occurs by means other than alteration of IkappaB-alpha kinetics. These data show for the first time that FRH promotes lung injury in part by increasing lung epithelial apoptosis. The enhanced apoptotic response might relate to FRH-mediated suppression of NF-kappaB activity in the alveolar epithelium with a resultant increase in susceptibility to TNF-alpha-mediated cell death.

Indexed as

AnimalsApoptosisBronchoalveolar Lavage FluidEpithelial CellsFeverFlow CytometryInflammationIn Situ Nick-End LabelingLipopolysaccharidesLung InjuryMaleMiceMice, Inbred C57BLNF-kappa BPulmonary AlveoliReverse Transcriptase Polymerase Chain ReactionLipopolysaccharidesNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID20200273
PMCPMC2865890
OpenAlexW2117737600

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.