Evidence map›Paper›PMID 29997122›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2018

Functional Evidence of Pulmonary Extracellular Vesicles in Infectious and Noninfectious Lung Inflammation.

Heedoo Lee, Duo Zhang, Debra L Laskin, Yang Jin

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
4.4field-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

81 citing papers in PubMed, 121 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Modulation of host inflammatory pathways byFrontiers in immunology · 2026
    Article
  7. Review
  8. Miconazole attenuates LPS-induced lung inflammation by modulating alveolar macrophage polarization via promoting lipid metabolic reprogramming.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  9. Review
  10. Lung contusion drives lung injury by modifying miRNA cargo in alveolar small extracellular vesicles.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  16. Extracellular Vesicle ASC: A Novel Mediator for Lung-Brain Axis in Preterm Brain Injury.American journal of respiratory cell and molecular biology · 2024
    Article
  17. Cell-cell communication: new insights and clinical implications.Signal transduction and targeted therapy · 2024
    Review
  18. Article
  19. Review
  20. Review

21 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

4 authors at 2 institutions in 1 country.

Heedoo LeeDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University, Boston, MA 02118; and.ORCID 0000-0002-2168-3643
Duo ZhangDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University, Boston, MA 02118; and.ORCID 0000-0003-0361-4174
Debra L LaskinDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854.
Yang JinDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Boston University, Boston, MA 02118; and yjin1@bu.edu.
Boston University · USRutgers, The State University of New Jersey · US

Funding

UMDNJ/Rutgers University CounterACT Research Center of ExcellenceU54AR055073 · NIAMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HECK, DIANE E · 2006 to 2024
$71.4M
Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ROBERT John LAUMBACH · 1988 to 2026
$47.4M
ACTIVATED MACROPHAGES AND OZONE TOXICITYR01ES004738 · NIEHS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI Debra L Laskin · 1989 to 2026
$9.0M
Cross talk between cav-1 and flot1 in lung injuryR01HL102076 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI JIN, YANG · 2011 to 2015
$2.1M
Development of the RNA molecule-enriched, cell type-specific exosomesR33AI121644 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI JIN, YANG · 2018 to 2020
$1.4M
Mechanistic insights of inflammation and organ failure after trauma or critical illnessR01GM127596 · NIGMS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI JIN, YANG · 2018 to 2021
$1.3M
Mechanistic insights into the systemic inflammation and organ failure in sepsisR01GM111313 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI JIN, YANG · 2014 to 2017
$1.3M
Development of the RNA molecule-enriched, cell type-specific exosomesR21AI121644 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI JIN, YANG · 2016 to 2017
$444k
NHLBI NIH HHS R01 HL102076NIAID NIH HHS R21 AI121644NIAID NIH HHS R33 AI121644NIAMS NIH HHS U54 AR055073NIEHS NIH HHS P30 ES005022NIEHS NIH HHS R01 ES004738NIGMS NIH HHS R01 GM111313NIGMS NIH HHS R01 GM127596
6 · The paper itself

Abstract

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a highly complex process that can be triggered by both noninfectious (sterile) and infectious stimuli. Inflammatory lung responses are one of the key features in the pathogenesis of this devastating syndrome. How ALI/ARDS-associated inflammation develops remains incompletely understood, particularly after exposure to sterile stimuli. Emerging evidence suggests that extracellular vesicles (EVs) regulate intercellular communication and inflammatory responses in various diseases. In this study, we characterized the generation and function of pulmonary EVs in the setting of ALI/ARDS, induced by sterile stimuli (oxidative stress or acid aspiration) and infection (LPS/Gram-negative bacteria) in mice. EVs detected in bronchoalveolar lavage fluid (BALF) were markedly increased after exposure of animals to both types of stimuli. After sterile stimuli, alveolar type-І epithelial cells were the main source of the BALF EVs. In contrast, infectious stimuli-induced BALF EVs were mainly derived from alveolar macrophages (AMs). Functionally, BALF EVs generated in both the noninfectious and infectious ALI models promoted the recruitment of macrophages in in vivo mouse models. Furthermore, BALF EVs differentially regulated AM production of cytokines and inflammatory mediators, as well as TLR expression in AMs in vivo. Regardless of their origin, BALF EVs contributed significantly to the development of lung inflammation in both the sterile and infectious ALI. Collectively, our results provide novel insights into the mechanisms by which EVs regulate the development of lung inflammation in response to diverse stimuli, potentially providing novel therapeutic and diagnostic targets for ALI/ARDS.

Indexed as

Acute Lung InjuryAnimalsExtracellular VesiclesInflammationLipopolysaccharidesLungMacrophages, AlveolarMicePneumoniaRespiratory Distress SyndromeLipopolysaccharides

Identifiers

PMID29997122
PMCPMC6109965
OpenAlexW2863980947

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.