Evidence map›Paper›PMID 26634656›Full record

ArticleScientific reports2015

Innate Immune Molecule Surfactant Protein D Attenuates Sepsis-induced Acute Pancreatic Injury through Modulating Apoptosis and NF-κB-mediated Inflammation.

Zhiyong Liu, Qiao Shi, Jiao Liu, Osama Abdel-Razek, Yongan Xu, Robert N Cooney, Guirong Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Intravenous surfactant protein D inhibits lipopolysaccharide-induced systemic inflammation.Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft · 2023
    Article
  6. Pyroptosis in acute pancreatitis and its therapeutic regulation.Apoptosis : an international journal on programmed cell death · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. 3Reactive oxygen species (Apex, N.C.) · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Collectins in urinary tract and kidney diseases.International urology and nephrology · 2018
    Review
  18. Review
  19. Article
  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

7 authors at 1 institution in 1 country.

Zhiyong LiuDepartment of Surgery, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
Qiao ShiDepartment of Surgery, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
Jiao LiuDepartment of Surgery, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
Osama Abdel-RazekDepartment of Surgery, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
Yongan XuDepartment of Surgery, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
Robert N CooneyDepartment of Surgery, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
Guirong WangDepartment of Surgery, SUNY Upstate Medical University, Syracuse, NY, 13210, USA.
SUNY Upstate Medical University · US

Funding

Mechanisms of 5'UTR splicing of human surfactant protein (SP)-A1 and SP-A2R21HL096007 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI WANG, GUIRONG · 2010 to 2011
$427k
NHLBI NIH HHS HL096007NHLBI NIH HHS R21 HL096007
6 · The paper itself

Abstract

Sepsis causes multiple-organ dysfunction including pancreatic injury, thus resulting in high mortality. Innate immune molecule surfactant protein D (SP-D) plays a critical role in host defense and regulating inflammation of infectious diseases. In this study we investigated SP-D functions in the acute pancreatic injury (API) with C57BL/6 Wild-type (WT) and SP-D knockout (KO) mice in cecal ligation and puncture (CLP) model. Our results confirm SP-D expression in pancreatic islets and intercalated ducts and are the first to explore the role of pancreatic SP-D in sepsis. CLP decreased pancreatic SP-D levels and caused severe pancreatic injury with higher serum amylase 24 h after CLP. Apoptosis and neutrophil infiltration were increased in the pancreas of septic KO mice (p < 0.05, vs septic WT mice), with lower Bcl-2 and higher caspase-3 levels in septic KO mice (p < 0.05). Molecular analysis revealed increased NF-κB-p65 and phosphorylated IκB-α levels along with higher serum levels of TNF-α and IL-6 in septic KO mice compared to septic WT mice (p < 0.01). Furthermore, in vitro islet cultures stimulated with LPS produced higher TNF-α and IL-6 (p < 0.05) from KO mice compared to WT mice. Collectively, these results demonstrate SP-D plays protective roles by inhibiting apoptosis and modulating NF-κB-mediated inflammation in CLP-induced API.

Indexed as

AnimalsApoptosisHumansImmunity, InnateInflammationInterleukin-6LigationMiceMice, KnockoutNF-kappa BPancreasPulmonary Surfactant-Associated Protein DPuncturesSepsisTumor Necrosis Factor-alphaInterleukin-6NF-kappa BPulmonary Surfactant-Associated Protein DTumor Necrosis Factor-alpha

Identifiers

PMID26634656
PMCPMC4669466
OpenAlexW2265208786

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.