Evidence map›Paper›PMID 19244200›Full record

ArticleAmerican journal of respiratory cell and molecular biology2009

The systemic inflammation of alveolar hypoxia is initiated by alveolar macrophage-borne mediator(s).

Jie Chao, John G Wood, Victor Gustavo Blanco, Norberto C Gonzalez

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 56 citations in OpenAlex.

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  12. MCPIP1 Regulates Alveolar Macrophage Apoptosis and Pulmonary Fibroblast Activation After in vitro Exposure to Silica.Toxicological sciences : an official journal of the Society of Toxicology · 2016
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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

4 authors at 1 institution in 1 country.

Jie ChaoDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
John G Wood
Victor Gustavo Blanco
Norberto C Gonzalez
University of Kansas Medical Center · US

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-39443
6 · The paper itself

Abstract

Alveolar hypoxia produces widespread systemic inflammation in rats. The inflammation appears to be triggered by activation of mast cells by a mediator released from alveolar macrophages, not by the reduced systemic partial pressure of oxygen (PO2). If this is correct, the following should apply: (1) neither mast cells nor tissue macrophages should be directly activated by hypoxia; and (2) mast cells should be activated when in contact with hypoxic alveolar macrophages, but not with hypoxic tissue macrophages. We sought here to determine whether hypoxia activates isolated alveolar macrophages, peritoneal macrophages, and peritoneal mast cells, and to study the response of the microcirculation to supernatants of these cultures. Rat mesenteric microcirculation intravital microscopy was combined with primary cultures of alveolar macrophages, peritoneal macrophages, and peritoneal mast cells. Supernatant of hypoxic alveolar macrophages, but not of hypoxic peritoneal macrophages, produced inflammation in mesentery. Hypoxia induced a respiratory burst in alveolar, but not peritoneal macrophages. Cultured peritoneal mast cells did not degranulate with hypoxia. Immersion of mast cells in supernatant of hypoxic alveolar macrophages, but not in supernatant of hypoxic peritoneal macrophages, induced mast cell degranulation. Hypoxia induced release of monocyte chemoattractant protein-1, a mast cell secretagogue, from alveolar, but not peritoneal macrophages or mast cells. We conclude that a mediator released by hypoxic alveolar macrophages activates mast cells and triggers systemic inflammation. Reduced systemic PO2 and activation of tissue macrophages do not play a role in this phenomenon. The inflammation could contribute to systemic effects of diseases featuring alveolar hypoxia.

Indexed as

Cell DegranulationParacrine CommunicationAnimalsCells, CulturedChemokine CCL2Culture Media, ConditionedHydrogen PeroxideHypoxiaInflammationInflammation MediatorsMacrophage ActivationMacrophages, AlveolarMacrophages, PeritonealMaleMast CellsMicrocirculationCcl2 protein, ratChemokine CCL2Culture Media, ConditionedHydrogen PeroxideInflammation MediatorsOxygen

Identifiers

PMID19244200
PMCPMC2778164
OpenAlexW2072920049

What OpenQuestion holds

Textmetadata
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.