Evidence map›Paper›PMID 30626665›Full record

ArticleJournal of virology2019

Unique Transcriptional Architecture in Airway Epithelial Cells and Macrophages Shapes Distinct Responses following Influenza Virus Infection

Joel Z Ma, Wy Ching Ng, Luke Zappia, Linden J Gearing, Moshe Olshansky, Kym Pham, Karey Cheong, Arthur Hsu, Stephen J Turner, Odilia Wijburg and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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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

13 authors at 4 institutions in 1 country.

Joel Z MaDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia intuitivelogic.au@gmail.com preading@unimelb.edu.au.
Wy Ching NgDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia.
Luke ZappiaDepartment of Pathology, University of Melbourne, Parkville, Victoria, Australia.
Linden J GearingCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Moshe OlshanskyDepartment of Microbiology, Monash University, Clayton, Victoria, Australia.
Kym PhamCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Karey CheongCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Arthur HsuCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Stephen J TurnerDepartment of Microbiology, Monash University, Clayton, Victoria, Australia.
Odilia WijburgDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia.
Sarah L LondriganDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia.
Andrew G BrooksDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia.
Patrick C ReadingDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria, Australia intuitivelogic.au@gmail.com preading@unimelb.edu.au.
University of Melbourne · AUMonash University · AUHudson Institute of Medical Research · AUPeter Doherty Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway epithelial cells and macrophages differ markedly in their responses to influenza A virus (IAV) infection. To investigate transcriptional responses underlying these differences, purified subsets of type II airway epithelial cells (ATII) and alveolar macrophages (AM) recovered from the lungs of mock- or IAV-infected mice at 9 h postinfection were subjected to RNA sequencing. This time point was chosen to allow for characterization of cell types first infected with the virus inoculum, prior to multicycle virus replication and the infiltration of inflammatory cells into the airways. In the absence of infection, AM predominantly expressed genes related to immunity, whereas ATII expressed genes consistent with their physiological roles in the lung. Following IAV infection, AM almost exclusively activated cell-intrinsic antiviral pathways that were dependent on interferon (IFN) regulatory factor 3/7 (IRF3/7) and/or type I IFN signaling. In contrast, IAV-infected ATII activated a broader range of physiological responses, including cell-intrinsic antiviral pathways, which were both independent of and dependent on IRF3/7 and/or type I IFN. These data suggest that transcriptional profiles hardwired during development are a major determinant underlying the different responses of ATII and AM to IAV infection.

Indexed as

Alveolar Epithelial CellsAnimalsCell LineCommunicable DiseasesDogsEpithelial CellsHumansInfluenza A Virus, H1N1 SubtypeInfluenza, HumanInterferon Regulatory Factor-3Interferon Regulatory Factor-7InterferonsLungMacrophagesMacrophages, AlveolarMadin Darby Canine Kidney CellsInterferon Regulatory Factor-3Interferon Regulatory Factor-7Interferonsepithelial cellinfluenzalungmacrophagemouse modelRNA sequencing

Identifiers

PMID30626665
PMCPMC6401432
OpenAlexW2910727896

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.