Evidence map›Paper›PMID 25786179›Full record

ArticleImmunity2015

Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection.

Jennifer Kearley, Jonathan S Silver, Caroline Sanden, Zheng Liu, Aaron A Berlin, Natalie White, Michiko Mori, Tuyet-Hang Pham, Christine K Ward, Gerard J Criner and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers.

0numbers the graph read from it
0cells of the map it votes in
201citing 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

201 citing papers in PubMed.

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141 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Jennifer KearleyDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune LLC, Gaithersburg, MD 20878, USA.
Jonathan S SilverDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune LLC, Gaithersburg, MD 20878, USA.
Caroline SandenDepartment of Experimental Medical Science, Lund University, Lund 22184, Sweden.
Zheng LiuDepartment of Translational Sciences, MedImmune LLC, Gaithersburg, MD 20878, USA.
Aaron A BerlinDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune LLC, Gaithersburg, MD 20878, USA.
Natalie WhiteDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune LLC, Gaithersburg, MD 20878, USA.
Michiko MoriDepartment of Experimental Medical Science, Lund University, Lund 22184, Sweden.
Tuyet-Hang PhamDepartment of Translational Sciences, MedImmune LLC, Gaithersburg, MD 20878, USA.
Christine K WardDepartment of Translational Sciences, MedImmune LLC, Gaithersburg, MD 20878, USA.
Gerard J CrinerPulmonary and Critical Care Medicine, Department of Medicine, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Nathaniel MarchettiPulmonary and Critical Care Medicine, Department of Medicine, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Tomas MustelinDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune LLC, Gaithersburg, MD 20878, USA.
Jonas S ErjefaltDepartment of Experimental Medical Science, Lund University, Lund 22184, Sweden.
Roland KolbeckDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune LLC, Gaithersburg, MD 20878, USA.
Alison A HumblesDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune LLC, Gaithersburg, MD 20878, USA. Electronic address: humblesa@medimmune.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease and is presumed to be central to the altered responsiveness to recurrent infection in these patients. We examined the effects of smoke priming underlying the exacerbated response to viral infection in mice. Lack of interleukin-33 (IL-33) signaling conferred complete protection during exacerbation and prevented enhanced inflammation and exaggerated weight loss. Mechanistically, smoke was required to upregulate epithelial-derived IL-33 and simultaneously alter the distribution of the IL-33 receptor ST2. Specifically, smoke decreased ST2 expression on group 2 innate lymphoid cells (ILC2s) while elevating ST2 expression on macrophages and natural killer (NK) cells, thus altering IL-33 responsiveness within the lung. Consequently, upon infection and release, increased local IL-33 significantly amplified type I proinflammatory responses via synergistic modulation of macrophage and NK cell function. Therefore, in COPD, smoke alters the lung microenvironment to facilitate an alternative IL-33-dependent exaggerated proinflammatory response to infection, exacerbating disease.

Indexed as

AnimalsFemaleGene Expression RegulationHumansImmunity, InnateInfluenza A virusInterleukin-1 Receptor-Like 1 ProteinInterleukin-33InterleukinsKiller Cells, NaturalLungLymphocytesMacrophagesMice, TransgenicNicotianaOrthomyxoviridae InfectionsIl1rl1 protein, mouseIl33 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33InterleukinsReceptors, InterleukinSmoke

Identifiers

PMID25786179

What OpenQuestion holds

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Read underepoch 390

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.