Evidence map›Paper›PMID 17384935›Full record

ArticleIntensive care medicine2007

Targeting caspase-1 by inhalation-therapy: effects of Ac-YVAD-CHO on IL-1 beta, IL-18 and downstream proinflammatory parameters as detected in rat endotoxaemia.

Kim A Boost, Sandra Hoegl, Christian Hofstetter, Michael Flondor, Klaus Stegewerth, Ilka Platacis, Josef Pfeilschifter, Heiko Muhl, Bernhard Zwissler

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Intensive care medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 13% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 57 citations in OpenAlex.

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  5. Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025
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  18. Inflammatory targets of therapy in sickle cell disease.Translational research : the journal of laboratory and clinical medicine · 2016
    Review
  19. The acute respiratory distress syndrome: from mechanism to translation.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Review
  20. 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

9 authors at 1 institution in 1 country.

Kim A BoostDepartment of Anaesthesiology, Intensive Care and Pain Therapy, University Hospital of Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany. k.boost@med.uni-frankfurt.de.
Sandra HoeglDepartment of Anaesthesiology, Intensive Care and Pain Therapy, University Hospital of Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Christian HofstetterDepartment of Anaesthesiology, Intensive Care and Pain Therapy, University Hospital of Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Michael FlondorDepartment of Anaesthesiology, Intensive Care and Pain Therapy, University Hospital of Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Klaus StegewerthDepartment of Anaesthesiology, Intensive Care and Pain Therapy, University Hospital of Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Ilka PlatacisDepartment of Anaesthesiology, Intensive Care and Pain Therapy, University Hospital of Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Josef PfeilschifterPharmazentrum Frankfurt/ZAFES, University Hospital of Johann Wolfgang Goethe-University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Heiko MuhlPharmazentrum Frankfurt/ZAFES, University Hospital of Johann Wolfgang Goethe-University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Bernhard ZwisslerDepartment of Anaesthesiology, Intensive Care and Pain Therapy, University Hospital of Johann Wolfgang Goethe University, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Germany.
Goethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWe set out to investigate whether the nebulized and inhaled specific caspase-1 inhibitor Ac-YVAD-CHO has the potential to attenuate the pulmonary and systemic release of the caspase-1-dependent cytokines interleukin-1 beta (IL-1 beta) and interleukin-18 (IL-18) as well as their downstream enzymes iNOS and COX-2 in rat experimental endotoxaemia. DESIGN AND

settingControlled, randomized animal study in a university research facility. SUBJECT: Male Sprague-Dawley rats (n=32) were randomly treated as follows: Inhaled Ac-YVAD-CHO was administered in eight rats at a inhaled total dosage of 5 mg and in eight rats at a inhaled total dose of 0.5 mg before infusion of lipopolysaccharide (LPS; 5 mg/kg, i.v.). Eight animals received LPS only. Eight animals served as controls without endotoxaemia. MEASUREMENTS AND

resultsAfter 4h of endotoxaemia, levels of IL-1 beta, IL-18 and TNF-alpha in plasma and bronchoalveolar fluid (BALF) were analyzed. Nitric oxide (NO) release from alveolar macrophages was measured by Griess assay. Amounts of iNOS protein in alveolar macrophages and COX-2 protein in lung homogenates were determined by Western blotting. Significant reductions in release of IL-1 beta (-58%, p<0.05) and IL-18 (-51%, p<0.05) in plasma and IL-1 beta (-59%, p<0.05) in BALF were found in animals pretreated with inhaled caspase-1 inhibitor compared with animals without therapy. Expression of iNOS in alveolar macrophages and COX-2 in lung tissue was concurrently decreased in the treatment groups compared with control animals.

conclusionsOur data demonstrate that administration of the caspase-1 inhibitor Ac-YVAD-CHO by inhalation is able to reduce the pulmonary and systemic release of proinflammatory mediators in rat endotoxaemia. These results further underscore that inhalation may constitute an effective route of anti-inflammatory drug administration, beneficial in the clinical setting of ARDS.

Indexed as

Caspase InhibitorsAdministration, InhalationAerosolsAnimalsBlood PressureCysteine Proteinase InhibitorsEndotoxemiaHeart RateInterleukin-18Interleukin-1betaMaleOligopeptidesRatsRats, Sprague-DawleyTumor Necrosis FactorsAerosolsCaspase InhibitorsCysteine Proteinase InhibitorsInterleukin-18Interleukin-1betaL 709049OligopeptidesTumor Necrosis Factors

Identifiers

PMID17384935
OpenAlexW2019669854

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.