Evidence map›Paper›PMID 19545431›Full record

ReviewRespiratory research2009

Alveolar hypoxia, alveolar macrophages, and systemic inflammation.

Jie Chao, John G Wood, Norberto C Gonzalez

Abstract readReview
In one paragraph

Review in Respiratory research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Review
  2. Review
  3. Atelectasis predicts poor prognosis in pediatric macrolides-unresponsiveFrontiers in cellular and infection microbiology · 2025
    Observational
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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.

Jie ChaoDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA. jchao@kumc.edu
John G Wood
Norberto C Gonzalez

Funding

OXYGEN TRANSPORT DURING EXERCISE IN PROLONGED HYPOXIAR01HL039443 · NHLBI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GONZALEZ, NORBERTO C. · 1988 to 2011
$2.4M
NHLBI NIH HHS HL 39443NHLBI NIH HHS R01 HL039443
6 · The paper itself

Abstract

Diseases featuring abnormally low alveolar PO2 are frequently accompanied by systemic effects. The common presence of an underlying inflammatory component suggests that inflammation may contribute to the pathogenesis of the systemic effects of alveolar hypoxia. While the role of alveolar macrophages in the immune and defense functions of the lung has been long known, recent evidence indicates that activation of alveolar macrophages causes inflammatory disturbances in the systemic microcirculation. The purpose of this review is to describe observations in experimental animals showing that alveolar macrophages initiate a systemic inflammatory response to alveolar hypoxia. Evidence obtained in intact animals and in primary cell cultures indicate that alveolar macrophages activated by hypoxia release a mediator(s) into the circulation. This mediator activates perivascular mast cells and initiates a widespread systemic inflammation. The inflammatory cascade includes activation of the local renin-angiotensin system and results in increased leukocyte-endothelial interactions in post-capillary venules, increased microvascular levels of reactive O2 species; and extravasation of albumin. Given the known extrapulmonary responses elicited by activation of alveolar macrophages, this novel phenomenon could contribute to some of the systemic effects of conditions featuring low alveolar PO2.

Indexed as

AnimalsHumansHypoxiaInflammationIschemiaLung DiseasesMacrophage ActivationMacrophages, AlveolarRats

Identifiers

PMID19545431
PMCPMC2705912

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.