Evidence map›Paper›PMID 28812547›Full record

ReviewMucosal immunology2018

Lung epithelial cells: therapeutically inducible effectors of antimicrobial defense.

M M Leiva-Juárez, J K Kolls, S E Evans

Open access · bronzeAbstract readReview
In one paragraph

Review in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
14.5field-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

142 citing papers in PubMed, 198 citations in OpenAlex.

  1. Article
  2. Beyond the epithelium: multicellular niches in lung regeneration and disease.American journal of physiology. Lung cellular and molecular physiology · 2026
    Review
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  12. Innate immune recognition ofCell surface (Amsterdam, Netherlands) · 2025
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  20. Article

82 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

3 authors at 2 institutions in 1 country.

M M Leiva-JuárezDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
J K KollsCenter for Translational Research in Infection and Inflammation, Tulane School of Medicine, New Orleans, Louisiana, USA.
S E EvansDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
The University of Texas MD Anderson Cancer Center · USTulane University · US

Funding

Th17 Cytokines and Lung ImmunityR37HL079142 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KOLLS, JAY K · 2010 to 2017
$3.6M
Inducible epithelial antiviral resistance to prevent asthmaDP2HL123229 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI EVANS, SCOTT E. · 2013 to 2013
$2.4M
Epithelial mechanisms of inducible resistance to AML-associated pneumoniaR01HL117976 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI EVANS, SCOTT E. · 2014 to 2018
$2.0M
NHLBI NIH HHS DP2 HL123229NHLBI NIH HHS R01 HL117976NHLBI NIH HHS R37 HL079142
6 · The paper itself

Abstract

Lung epithelial cells are increasingly recognized to be active effectors of microbial defense, contributing to both innate and adaptive immune function in the lower respiratory tract. As immune sentinels, lung epithelial cells detect diverse pathogens through an ample repertoire of membrane-bound, endosomal, and cytosolic pattern-recognition receptors (PRRs). The highly plastic epithelial barrier responds to detected threats via modulation of paracellular flux, intercellular communications, mucin production, and periciliary fluid composition. Epithelial PRR stimulation also induces production of cytokines that recruit and sculpt leukocyte-mediated responses, and promotes epithelial generation of antimicrobial effector molecules that are directly microbicidal. The epithelium can alternately enhance tolerance to pathogens, preventing tissue damage through PRR-induced inhibitory signals, opsonization of pathogen-associated molecular patterns, and attenuation of injurious leukocyte responses. The inducibility of these protective responses has prompted attempts to therapeutically harness epithelial defense mechanisms to protect against pneumonias. Recent reports describe successful strategies for manipulation of epithelial defenses to protect against a wide range of respiratory pathogens. The lung epithelium is capable of both significant antimicrobial responses that reduce pathogen burdens and tolerance mechanisms that attenuate immunopathology. This manuscript reviews inducible lung epithelial defense mechanisms that offer opportunities for therapeutic manipulation to protect vulnerable populations against pneumonia.

Indexed as

AnimalsAnti-Infective AgentsHumansImmune ToleranceImmunityImmunocompromised HostPneumoniaReceptors, Pattern RecognitionRespiratory MucosaUp-RegulationAnti-Infective AgentsReceptors, Pattern Recognition

Identifiers

PMID28812547
PMCPMC5738267
OpenAlexW2746600415

What OpenQuestion holds

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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.