Evidence map›Paper›PMID 33563839›Full record

ArticlemBio2021

Hemozoin Promotes Lung Inflammation via Host Epithelial Activation.

Shivang S Shah, David A Fidock, Alice S Prince

Open access · goldAbstract read
In one paragraph

Article in mBio, 2021. 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
1.0field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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 1 institution in 1 country.

Shivang S ShahDivision of Infectious Diseases, Department of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, New York, USA ss5235@columbia.edu.ORCID 0000-0001-6399-8160
David A FidockDivision of Infectious Diseases, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York, USA.ORCID 0000-0001-6753-8938
Alice S PrinceDivision of Infectious Diseases, Department of Pediatrics, College of Physicians and Surgeons, Columbia University, New York, New York, USA.
Columbia University · US

Funding

Innate Immune Clearance of Host-Adapted Pulmonary PathogensR35HL135800 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PRINCE, ALICE S · 2017 to 2023
$5.9M
Role of pfcrt in chloroquine resistance in P. falciparumR01AI050234 · NIAID · YESHIVA UNIVERSITY · PI FIDOCK, DAVID A · 2001 to 2015
$5.7M
Leveraging PfCRT Structure to Discern Function and Predict Emergence of Drug-Resistant MalariaR01AI147628 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI David A Fidock, Filippo Mancia · 2019 to 2026
$5.1M
Defining the Role of PfCRT and PfMDR1 as Pleiotropic Mediators of Plasmodium falciparum Multidrug ResistanceR37AI050234 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI David A Fidock · 2018 to 2026
$4.4M
Defining P. falciparum resistance to artemisinin-based combination therapiesR01AI109023 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI FIDOCK, DAVID A · 2014 to 2025
$4.4M
Elucidating the molecular basis of piperaquine resistance in Plasmodium falciparumR01AI124678 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI David A Fidock · 2016 to 2026
$4.3M
Training in Pediatric Infectious DiseasesT32AI007531 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PRINCE, ALICE S, SAIMAN, LISA · 1998 to 2023
$4.0M
Becton Dickinson LSR II Analytical Flow CytometerS10RR027050 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CLYNES, RAPHAEL A. · 2011 to 2011
$413k
NCRR NIH HHS S10 RR027050NHLBI NIH HHS R35 HL135800NIAID NIH HHS R01 AI050234NIAID NIH HHS R01 AI109023NIAID NIH HHS R01 AI124678NIAID NIH HHS R01 AI147628NIAID NIH HHS R37 AI050234NIAID NIH HHS T32 AI007531
6 · The paper itself

Abstract

Respiratory distress in severe malaria is associated with high mortality, but its pathogenesis remains unclear. The malaria pigment hemozoin (HZ) is abundant in target organs of severe malaria, including the lungs, and is known to be a potent innate immune activator of phagocytes. We hypothesized that HZ might also stimulate lung epithelial activation and thereby potentiate lung inflammation. We show here that airway epithelium stimulated with HZ undergoes global transcriptional reprogramming and changes in cell surface protein expression that comprise an epithelial activation phenotype. Proinflammatory signaling is induced, and key cytoadherence molecules are upregulated, including several associated with severe malaria, such as CD36 and ICAM1. Epithelial and extracellular matrix remodeling pathways are transformed, including induction of key metalloproteases and modulation of epithelial junctions. The overall program induced by HZ serves to promote inflammation and neutrophil transmigration, and is recapitulated in a murine model of HZ-induced acute pneumonitis. Together, our data demonstrate a direct role for hemozoin in stimulating epithelial activation that could potentiate lung inflammation in malaria.

Indexed as

Host-Parasite InteractionsAnimalsBronchiCD36 AntigensCell LineCell MovementEpithelial CellsFemaleGene Expression ProfilingHemeproteinsInflammationIntercellular Adhesion Molecule-1LungMalaria, FalciparumMiceMice, Inbred C57BLCD36 AntigensHemeproteinshemozoinIcam1 protein, mouseIntercellular Adhesion Molecule-1hemozoinlung inflammationmalaria

Identifiers

PMID33563839
PMCPMC7885402
OpenAlexW3127119951

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.