Evidence map›Paper›PMID 42337236›Full record

ArticleNature communications2026

Pulmonary inflammation in severe pneumonia is characterised by compartmentalised and mechanistically distinct sub-phenotypes.

Mark Jeffrey, Josefin Bartholdson Scott, Shyamanova Mazumdar, Richard J White, Ellen Higginson, Mailis Maes, Sally Forrest, Joana Pereira-Dias, Surendra Parmar, Emma Heasman-Hunt and 13 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
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

23 authors.

Mark JeffreyDivision of Perioperative, Acute, Critical Care and Emergency Medicine, Department of Medicine, University of Cambridge, Cambridge, UK.
Josefin Bartholdson Scott *Cambridge Institute of Therapeutic Immunology & Infectious Disease, Department of Medicine, University of Cambridge, Cambridge, UK.ORCID 0000-0003-3380-4446
Shyamanova Mazumdar *Division of Perioperative, Acute, Critical Care and Emergency Medicine, Department of Medicine, University of Cambridge, Cambridge, UK.ORCID 0009-0009-9692-9562
Richard J WhiteCambridge Institute of Therapeutic Immunology & Infectious Disease, Department of Medicine, University of Cambridge, Cambridge, UK.ORCID 0000-0003-1842-412X
Ellen HigginsonCambridge Institute of Therapeutic Immunology & Infectious Disease, Department of Medicine, University of Cambridge, Cambridge, UK.
Mailis MaesCambridge Institute of Therapeutic Immunology & Infectious Disease, Department of Medicine, University of Cambridge, Cambridge, UK.
Sally ForrestCambridge Institute of Therapeutic Immunology & Infectious Disease, Department of Medicine, University of Cambridge, Cambridge, UK.
Joana Pereira-DiasCambridge Institute of Therapeutic Immunology & Infectious Disease, Department of Medicine, University of Cambridge, Cambridge, UK.
Surendra ParmarClinical Microbiology and Public Health Laboratory, UK Health Security Agency, Cambridge, UK.
Emma Heasman-HuntClinical Microbiology and Public Health Laboratory, UK Health Security Agency, Cambridge, UK.
Martin D CurranClinical Microbiology and Public Health Laboratory, UK Health Security Agency, Cambridge, UK.
Petra PolgarovaJohn V Farman Intensive Care Unit, Addenbrooke's Hospital, Cambridge, UK.
Jurgen HerreDepartment of Respiratory Medicine, Addenbrooke's Hospital, Cambridge, UK.
Els WautersLaboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Department of Chronic Diseases and Metabolism, KU Leuven, Leuven, Belgium.
Diether LambrechtsLaboratory of Translational Genetics, Department of Human Genetics, KU Leuven, Leuven, Belgium.ORCID 0000-0002-3429-302X
Pierre Van MolDepartment of Pneumology, University Hospitals Leuven, Leuven, Belgium.
Cato JacobsLaboratory for Clinical Infectious and Inflammatory Disorders, Department of Microbiology, Immunology and Transplantation, KU Leuven, Leuven, Belgium.
Joost WautersLaboratory for Clinical Infectious and Inflammatory Disorders, Department of Microbiology, Immunology and Transplantation, KU Leuven, Leuven, Belgium.ORCID 0000-0002-5983-3897
Emma E DavenportWellcome Sanger Institute, Wellcome Genome Campus, Hinxton, UK.
Stephen BakerA*STAR Infectious Diseases Labs (A*STAR IDL), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Gordon DouganCambridge Institute of Therapeutic Immunology & Infectious Disease, Department of Medicine, University of Cambridge, Cambridge, UK.
Vilas NavapurkarJohn V Farman Intensive Care Unit, Addenbrooke's Hospital, Cambridge, UK.
Andrew Conway MorrisDivision of Perioperative, Acute, Critical Care and Emergency Medicine, Department of Medicine, University of Cambridge, Cambridge, UK. ac926@cam.ac.uk.ORCID 0000-0002-3211-3216

Funding

CUH | Addenbrooke's Charitable Trust, Cambridge University Hospitals (Addenbrooke's Charitable Trust, Cambridge University Hospitals NHS Foundation Trust) ACT 900361RCUK | Medical Research Council (MRC) MR/V006118/1RCUK | MRC | Medical Research Foundation MR W006650/1Vlaams Instituut voor Biotechnologie (Flanders Institute for Biotechnology) VR 20162312 Doc.1512/4Wellcome Trust (Wellcome) 220540/Z/20/AWellcome Trust (Wellcome) WT 2055214/Z/16/Z
6 · The paper itself

Abstract

Pneumonia is the leading infectious disease killer worldwide and commonly requires admission to critical care. Despite its prevalence, the underpinning biology of severe pneumonia remains incompletely understood. Here we perform multifaceted assessments of bronchoalveolar transcriptome, cytokines, microbiology, and clinical features to biologically characterise a cohort of patients with suspected severe pneumonia. Our data implicate three lung-restricted transcriptionally defined severe pneumonia endotypes (termed 'Pneumotypes' (Pn)). All three Pneumotypes have comparable clinical presentations and severity of respiratory failure but experience divergent outcomes. Pn1, the most common, is characterised by low alveolar cytokines, expanded tolerogenic macrophages and epithelial damage. Pn3 is characterised by immature neutrophil infiltration, IL-6-STAT3 activation and longer duration of mechanical ventilation. Pn2 displays the fastest resolution, exhibiting a balanced immune response and epithelial-endothelial repair signatures. We identify and validate mechanistically distinct phenotypes in the lungs of patients with suspected pneumonia and acute lung injury, implicating targets for personalised therapy.

Indexed as

PneumoniaAcute Lung InjuryBronchoalveolar Lavage FluidCytokinesFemaleHumansInterleukin-6LungMaleNeutrophil InfiltrationNeutrophilsPhenotypeSTAT3 Transcription FactorTranscriptomeCytokinesInterleukin-6STAT3 Transcription Factor

Identifiers

PMID42337236
PMCPMC13291267

What OpenQuestion holds

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Registered trials

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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.