Evidence map›Paper›PMID 26371253›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Acute-Phase Deaths from Murine Polymicrobial Sepsis Are Characterized by Innate Immune Suppression Rather Than Exhaustion.

Evan L Chiswick, Juan R Mella, John Bernardo, Daniel G Remick

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Dysregulation of neutrophil in sepsis: recent insights and advances.Cell communication and signaling : CCS · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. IRF3 Signaling within the Mouse Stroma Influences Sepsis Pathogenesis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  11. Aged IRF3-KO Mice are Protected from Sepsis.Journal of inflammation research · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Premise for Standardized Sepsis Models.Shock (Augusta, Ga.) · 2019
    Article
  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

4 authors at 3 institutions in 1 country.

Evan L ChiswickDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118;
Juan R MellaDepartment of Surgery, Boston University Medical Center, Boston, MA 02118; and.
John BernardoDivision of Pulmonary, Allergy, and Critical Care Medicine, Boston University Medical Center, Boston, MA 02118.
Daniel G RemickDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118; remickd@bu.edu.
Boston University · USBoston Medical Center · USUniversity Medical Center · US

Funding

RESEARCH TRAINING IN IMMUNOLOGYT32AI007309 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GUMMULURU, SURYARAM · 1988 to 2024
$7.4M
RESEARCH TRAINING IN BLOOD DISEASES AND RESOURCEST32HL007501 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LERNER, ADAM, STEINBERG, MARTIN H. · 1985 to 2018
$5.4M
Impact of Biological, Clinical, and Social Determinants on Trauma and Trauma OutcomesT32GM086308 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Alik Farber, Daniel G. Remick · 2010 to 2026
$3.5M
Adenosine and Oxygen Modulate Antimicrobial DefensesR01GM097320 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI REMICK, DANIEL G., SITKOVSKY, MICHAIL · 2011 to 2014
$1.2M
Mechanisms of phagocytic cell defects induced by inhibitory IgGR21AI112887 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI REMICK, DANIEL G. · 2014 to 2015
$450k
NHLBI NIH HHS T32 HL007501NHLBI NIH HHS T32HL007501NIAID NIH HHS R21 AI112887NIAID NIH HHS R21AI112887NIAID NIH HHS T32 AI007309NIAID NIH HHS T32AI007309NIGMS NIH HHS R01 GM097320NIGMS NIH HHS R01GM97320NIGMS NIH HHS T32 GM086308NIGMS NIH HHS T32GM86308
6 · The paper itself

Abstract

Sepsis, a leading cause of death in the United States, has poorly understood mechanisms of mortality. To address this, our model of cecal ligation and puncture (CLP) induced sepsis stratifies mice as predicted to Live (Live-P) or Die (Die-P) based on plasma IL-6. Six hours post-CLP, both Live-P and Die-P groups have equivalent peritoneal bacterial colony forming units and recruitment of phagocytes. By 24 h, however, Die-P mice have increased bacterial burden, despite increased neutrophil recruitment, suggesting Die-P phagocytes have impaired bacterial killing. Peritoneal cells were used to study multiple bactericidal processes: bacterial killing, reactive oxygen species (ROS) generation, and phagocytosis. Total phagocytosis and intraphagosomal processes were determined with triple-labeled Escherichia coli, covalently labeled with ROS- and pH-sensitive probes, and an ROS/pH-insensitive probe for normalization. Although similar proportions of Live-P and Die-P phagocytes responded to exogenous stimuli, Die-P phagocytes showed marked deficits in all parameters measured, thus suggesting immunosuppression rather than exhaustion. This contradicts the prevailing sepsis paradigm that acute-phase sepsis deaths (<5 d) result from excessive inflammation, whereas chronic-phase deaths (>5 d) are characterized by insufficient inflammation and immunosuppression. These data suggest that suppression of cellular innate immunity in sepsis occurs within the first 6 h.

Indexed as

PhagocytosisAcute-Phase ReactionAnimalsEscherichia coliEscherichia coli InfectionsFemaleInterleukin-6MiceMice, Inbred ICRReactive Oxygen SpeciesSepsisInterleukin-6Reactive Oxygen Species

Identifiers

PMID26371253
PMCPMC4592823
OpenAlexW2177625501

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.