Evidence map›Paper›PMID 22064428›Full record

ReviewNature medicine2011

The neutrophil in vascular inflammation.

Mia Phillipson, Paul Kubes

Abstract readReview
In one paragraph

Review in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 400 papers.

0numbers the graph read from it
0cells of the map it votes in
400citing papers in PubMed
–field-weighted citation impact
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

400 citing papers in PubMed.

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340 more citing papers are in PubMed but not listed here.

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

2 authors.

Mia PhillipsonDepartment of Medical Cell Biology, Division of Integrative Physiology, Uppsala University, Uppsala, Sweden.
Paul Kubes

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Here we focus on how neutrophils have a key regulatory role in vascular inflammation. Recent studies using advanced imaging techniques have yielded new insights into the mechanisms by which neutrophils contribute to defense against bacterial infections and also against sterile injury. In these settings, neutrophils are recruited by various mechanisms depending on the situation. We also describe how these processes may be disrupted in systemic infections, with a particular emphasis on mouse models of sepsis. Neutrophils are often immobilized in the lungs and liver during systemic infections, and this immobilization may be a mechanism through which bacteria can evade the innate immune response or allow neutrophils to form neutrophil extracellular traps that trap and kill bacteria in blood. The platelet is also an important player in sepsis, and we describe how it collaborates with neutrophils in the formation of neutrophil extracellular traps.

Indexed as

BacteriaBacterial InfectionsBlood VesselsChemotaxis, LeukocyteHumansNeutrophil ActivationNeutrophilsp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPTEN PhosphohydrolaseVasculitisp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPTEN Phosphohydrolase

Identifiers

PMID22064428
PMCPMC7095830

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.