Evidence map›Paper›PMID 36193662›Full record

ReviewJournal of leukocyte biology2022

Immunopathology of chronic critical illness in sepsis survivors: Role of abnormal myelopoiesis.

Jaimar C Rincon, Philip A Efron, Lyle L Moldawer

Open access · greenAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. NuclearJournal of clinical & cellular immunology · 2025
    Article
  7. Article
  8. Article
  9. Observational
  10. Article
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  12. Review
  13. Article
  14. Article
  15. Here, There, and Everywhere: Myeloid-Derived Suppressor Cells in Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Review
  16. 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

3 authors at 2 institutions in 1 country.

Jaimar C RinconSepsis and Critical Illness Research Center, Laboratory of Inflammation Biology and Surgical Science, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Philip A EfronSepsis and Critical Illness Research Center, Laboratory of Inflammation Biology and Surgical Science, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
Lyle L MoldawerSepsis and Critical Illness Research Center, Laboratory of Inflammation Biology and Surgical Science, Department of Surgery, University of Florida College of Medicine, Gainesville, Florida, USA.
University of Florida · USFlorida College · US

Funding

University of Florida Older Americans Independence Center (OAIC)P30AG028740 · NIA · UNIVERSITY OF FLORIDA · PI CHRISTIAAN LEEUWENBURGH · 2007 to 2026
$22.8M
Renewal: Dysfunctional Myelopoiesis and Myeloid-Derived Suppressor Cells in Sepsis PathobiologyRM1GM139690 · NIGMS · UNIVERSITY OF FLORIDA · PI Philip A Efron, Michael Paul Kladde · 2021 to 2026
$10.3M
R35 Equipment SupplementR35GM140806 · NIGMS · UNIVERSITY OF FLORIDA · PI EFRON, PHILIP A · 2021 to 2025
$2.2M
NIA NIH HHS P30 AG028740NIGMS NIH HHS R35 GM140806NIGMS NIH HHS RM1 GM139690
6 · The paper itself

Abstract

Sepsis remains the single most common cause of mortality and morbidity in hospitalized patients requiring intensive care. Although earlier detection and improved treatment bundles have reduced in-hospital mortality, long-term recovery remains dismal. Sepsis survivors who experience chronic critical illness often demonstrate persistent inflammation, immune suppression, lean tissue wasting, and physical and functional cognitive declines, which often last in excess of 1 year. Older patients and those with preexisting comorbidities may never fully recover and have increased mortality compared with individuals who restore their immunologic homeostasis. Many of these responses are shared with individuals with advanced cancer, active autoimmune diseases, chronic obstructive pulmonary disease, and chronic renal disease. Here, we propose that this resulting immunologic endotype is secondary to a persistent maladaptive reprioritization of myelopoiesis and pathologic activation of myeloid cells. Driven in part by the continuing release of endogenous alarmins from chronic organ injury and muscle wasting, as well as by secondary opportunistic infections, ongoing myelopoiesis at the expense of lymphopoiesis and erythropoiesis leads to anemia, recurring infections, and lean tissue wasting. Early recognition and intervention are required to interrupt this pathologic activation of myeloid populations.

Indexed as

Critical IllnessSepsisChronic DiseaseHumansMyelopoiesisNeoplasm Recurrence, LocalSurvivorsbone marrowCCIemergency myelopoiesissepsissepsis survivors

Identifiers

PMID36193662
PMCPMC9701155
OpenAlexW4301391639

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.