Evidence map›Paper›PMID 31488203›Full record

ArticleJournal of translational medicine2019

Aryl hydrocarbon receptor ligands enhance lung immunity through intestinal IKKβ pathways.

Tzyy-Bin Tsay, Pei-Hsuan Chen, Lee-Wei Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

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  6. Disease tolerance: a protective mechanism of lung infections.Frontiers in cellular and infection microbiology · 2023
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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 at 3 institutions in 1 country.

Tzyy-Bin TsayDepartment of Surgery, Kaohsiung Armed Forces General Hospital Zuoying Branch, Kaohsiung, Taiwan.
Pei-Hsuan ChenDepartment of Surgery, Kaohsiung Veterans General Hospital, No.386, Ta-chung 1st Road, Kaohsiung, 813, Taiwan.
Lee-Wei ChenDepartment of Surgery, Kaohsiung Veterans General Hospital, No.386, Ta-chung 1st Road, Kaohsiung, 813, Taiwan. lwchen@vghks.gov.tw.ORCID 0000-0002-3583-1248
Kaohsiung Armed Forces General Hospital · TWKaohsiung Veterans General Hospital · TWNational Sun Yat-sen University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInfection by antibiotic-resistant microorganisms is common in intensive care units and has become a global problem. Here, we determined the effect of aryl hydrocarbon receptor (AhR) stimulation on antibiotics-induced systemic defense impairment and its mechanisms.

methodsC57BL/6 wild-type (WT) mice received combined antibiotics with or without Ahr ligands (tryptophan and indole), or dead Lactobacillus plantarum supplementation. The defense mechanisms against Pseudomonas aeruginosa infection in the lung were examined.

resultsAntibiotic treatments decreased the phagocytic activity, physiological activity, and the peroxynitrite production of alveolar macrophage (AMs). It also enhanced P. aeruginosa pneumonia-induced bacterial counts in the lung. Tryptophan and dead L. plantarum supplementation reversed antibiotic-induced intracellular adhesion molecule (ICAM) as well as IL-6 expression, and increased P. aeruginosa pneumonia-induced bacterial counts in the lung and increased phagocytic activity and peroxynitrite production of AMs. Moreover, these treatments reversed the antibiotics-induced reduction of Ahr expression, antibacterial proteins, reactive oxygen species (ROS) production, and NF-κB DNA binding activity of the intestinal mucosa and plasma IL-6 levels. P. aeruginosa counts increased and phagocytic activity of AMs and myeloperoxidase (MPO) activity decreased in intestinal IKKβ depleted mice. Antibiotics, antibiotic with tryptophan feeding, or antibiotic with dead L. plantarum feeding treatments did not change the phagocytic activity and peroxynitrite production of AMs, plasma IL-6 levels, and the expression of Ahr of intestine in intestinal IKKβ depleted mice.

conclusionAntibiotic treatment impairs lung immune defenses by decreasing Ahr expression in the intestine and peroyxnitrite production of the AMs. Ahr ligands reverses antibiotic-induced lung defense against bacterial infection through intestinal ROS production and NF-κB activation. The gut is critical in maintaining lung defense mechanism through the intestinal IKKβ pathways.

Indexed as

Signal TransductionAdministration, OralAnimalsAnti-Bacterial AgentsColony Count, MicrobialI-kappa B KinaseIndolesIntestinal MucosaIntestinesLactiplantibacillus plantarumLigandsLungMacrophages, AlveolarMice, Inbred C57BLNF-kappa BPeroxynitrous AcidAnti-Bacterial AgentsI-kappa B KinaseindoleIndolesLigandsNF-kappa BPeroxynitrous AcidReactive Oxygen SpeciesReceptors, Aryl HydrocarbonTryptophanAlveolar macrophageNF-κBPeroxynitriteReactive oxygen speciesTryptophan

Identifiers

PMID31488203
PMCPMC6727541
OpenAlexW2971475134

What OpenQuestion holds

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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.