Evidence map›Paper›PMID 27782333›Full record

ReviewImmunological reviews2016

The immune system's role in sepsis progression, resolution, and long-term outcome.

Matthew J Delano, Peter A Ward

Open access · bronzeAbstract readReview
In one paragraph

Review in Immunological reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 517 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
517citing papers in PubMed, 6 pooled it
26.5field-weighted citation impact, top 1% 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

517 citing papers in PubMed, 6 syntheses or guidelines pooled it, 826 citations in OpenAlex.

  1. Clinical lipidomics in bacterial sepsis: a systematic review of serum and plasma evaluations.Metabolomics : Official journal of the Metabolomic Society · 2026
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

457 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 at 1 institution in 1 country.

Matthew J DelanoDepartment of Surgery, Division of Acute Care Surgery, University of Michigan, Ann Arbor, MI, USA.
Peter A WardDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA. pward@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Regulation of Lung Inflammation by Catecholamines and Adrenergic ReceptorsR01GM029507 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 1985 to 2013
$3.9M
Protective Effects of Anti-C5a in SepsisR01GM061656 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 2002 to 2013
$3.8M
LUNG INJURY BY OXYGEN METABOLITESR37GM029507 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 1987 to 1996
–
NIGMS NIH HHS R01 GM029507NIGMS NIH HHS R01 GM061656NIGMS NIH HHS R37 GM029507
6 · The paper itself

Abstract

Sepsis occurs when an infection exceeds local tissue containment and induces a series of dysregulated physiologic responses that result in organ dysfunction. A subset of patients with sepsis progress to septic shock, defined by profound circulatory, cellular, and metabolic abnormalities, and associated with a greater mortality. Historically, sepsis-induced organ dysfunction and lethality were attributed to the complex interplay between the initial inflammatory and later anti-inflammatory responses. With advances in intensive care medicine and goal-directed interventions, early 30-day sepsis mortality has diminished, only to steadily escalate long after "recovery" from acute events. As so many sepsis survivors succumb later to persistent, recurrent, nosocomial, and secondary infections, many investigators have turned their attention to the long-term sepsis-induced alterations in cellular immune function. Sepsis clearly alters the innate and adaptive immune responses for sustained periods of time after clinical recovery, with immune suppression, chronic inflammation, and persistence of bacterial representing such alterations. Understanding that sepsis-associated immune cell defects correlate with long-term mortality, more investigations have centered on the potential for immune modulatory therapy to improve long-term patient outcomes. These efforts are focused on more clearly defining and effectively reversing the persistent immune cell dysfunction associated with long-term sepsis mortality.

Indexed as

Immune SystemImmunityImmunomodulationAnimalsDisease ProgressionHumansImmunosuppression TherapyInflammationSecondary PreventionSepsisTime FactorsTreatment Outcomeadaptive immune dysfunctionimmune suppression sepsisinflammationinnate immune dysfunctionsepsis

Identifiers

PMID27782333
PMCPMC5111634
OpenAlexW2540365220

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.