Evidence map›Paper›PMID 21937948›Full record

ArticleShock (Augusta, Ga.)2011

Bacterial DNA induces pulmonary damage via TLR-9 through cross-talk with neutrophils.

Kiyoshi Itagaki, Yasaman Adibnia, Shiqin Sun, Cong Zhao, Tolga Sursal, Yu Chen, Wolfgang Junger, Carl J Hauser

Abstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-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.

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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  6. Pseudomonas aeruginosa biofilm is a potent inducer of phagocyte hyperinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
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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

8 authors at 4 institutions in 3 countries.

Kiyoshi ItagakiDepartment of Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA. kitagaki@bidmc.harvard.edu
Yasaman Adibnia
Shiqin Sun
Cong Zhao
Tolga Sursal
Yu Chen
Wolfgang Junger
Carl J Hauser
Beth Israel Deaconess Medical Center · USDaqing City People's Hospital · CNEastern Virginia Medical School · USIstanbul University · TR

Funding

Sphingosine 1-phosphate and PMN Ca2+ entry in traumaR01GM059179 · NIGMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI HAUSER, CARL J · 2000 to 2009
$2.7M
Mitochondrial DAMPs and Inflammation after injuryR01GM089711 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HAUSER, CARL J · 2010 to 2013
$1.7M
NIGMS NIH HHS R01 GM059179NIGMS NIH HHS R01GM059179NIGMS NIH HHS R01 GM089711
6 · The paper itself

Abstract

Bacterial DNA (bDNA) contains hypomethylated "CpG" repeats that can be recognized by Toll-like receptor 9 (TLR-9) as a pathogen-associated molecular pattern. The ability of bDNA to initiate lung injury via TLR-9 has been inferred on the basis of studies using artificial CpG DNA. But the role of authentic bDNA in lung injury is still unknown. Moreover, the mechanisms by which CpG DNA species can lead to pulmonary injury are unknown, although neutrophils (PMNs) are thought to play a key role in the genesis of septic acute lung injury. We evaluated the effects of bDNA on PMN-endothelial cell (EC) interactions thought critical for initiation of acute lung injury. Using a biocapacitance system to monitor real-time changes in endothelial permeability, we demonstrate here that bDNA causes EC permeability in a dose-dependent manner uniquely in the presence of PMNs. These permeability changes are inhibited by chloroquine, suggesting TLR-9 dependency. When PMNs were preincubated with bDNA and applied to ECs or when bDNA was applied to ECs without PMNs, no permeability changes were detected. To study the underlying mechanisms, we evaluated the effects of bDNA on PMN-EC adherence. Bacterial DNA significantly increased PMN adherence to ECs in association with upregulated adhesion molecules in both cell types. Taken together, our results strongly support the conclusion that bDNA can initiate lung injury by stimulating PMN-EC adhesive interactions predisposing to endothelial permeability. Bacterial DNA stimulation of TLR-9 appears to promote enhanced gene expression of adhesion molecules in both cell types. This leads to PMN-EC cross-talk, which is required for injury to occur.

Indexed as

CD11b AntigenCD18 AntigensCell AdhesionCell LineCells, CulturedDNA, BacterialEndothelial CellsEndothelium, VascularE-SelectinHumansIntercellular Adhesion Molecule-1NeutrophilsToll-Like Receptor 9CD11b AntigenCD18 AntigensDNA, BacterialE-SelectinIntercellular Adhesion Molecule-1TLR9 protein, humanToll-Like Receptor 9

Identifiers

PMID21937948
PMCPMC3220777
OpenAlexW1985945544

What OpenQuestion holds

Textmetadata
LicenceTDM
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.