Evidence map›Paper›PMID 29958012›Full record

ArticleAmerican journal of respiratory cell and molecular biology2018

CARMA3 Mediates Allergic Lung Inflammation in Response to Alternaria alternata.

Benjamin Causton, Ana Pardo-Saganta, Jacob Gillis, Katherine Discipio, Tristan Kooistra, Jayaraj Rajagopal, Ramnik J Xavier, Josalyn L Cho, Benjamin D Medoff

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2018. 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
1.5field-weighted citation impact, top 19% 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.

  1. Trial
  2. Article
  3. Article
  4. The role of the CBM complex in allergic inflammation and disease.The Journal of allergy and clinical immunology · 2022
    Review
  5. Review
  6. Purified Native and Recombinant MajorJournal of fungi (Basel, Switzerland) · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Benjamin Causton1 Division of Pulmonary and Critical Care Medicine.
Ana Pardo-Saganta1 Division of Pulmonary and Critical Care Medicine.
Jacob Gillis1 Division of Pulmonary and Critical Care Medicine.
Katherine Discipio1 Division of Pulmonary and Critical Care Medicine.
Tristan Kooistra1 Division of Pulmonary and Critical Care Medicine.
Jayaraj Rajagopal1 Division of Pulmonary and Critical Care Medicine.
Ramnik J Xavier5 Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts; and.
Josalyn L Cho1 Division of Pulmonary and Critical Care Medicine.
Benjamin D Medoff1 Division of Pulmonary and Critical Care Medicine.ORCID 0000-0002-2558-0449
Pulmonary and Critical Care Associates · USHarvard University · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
Research Training in Pulmonary Immunology and Allergy at MGHT32HL116275 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI David C Christiani, ANDREW D LUSTER · 2013 to 2026
$8.6M
NHLBI NIH HHS T32 HL116275NIDDK NIH HHS P30 DK043351
6 · The paper itself

Abstract

The airway epithelial cell (AEC) response to allergens helps initiate and propagate allergic inflammation in asthma. CARMA3 is a scaffold protein that mediates G protein-coupled receptor-induced NF-κB activation in airway epithelium. In this study, we demonstrate that mice with CARMA3-deficient AECs have reduced airway inflammation, as well as reduced type 2 cytokine levels in response to Alternaria alternata. These mice also have reduced production of IL-33 and IL-25, and reduced numbers of innate lymphoid cells in the lung. We also show that CARMA3-deficient human AECs have decreased production of proasthmatic mediators in response to A. alternata. Finally, we show that CARMA3 interacts with inositol 1,4,5-trisphosphate receptors in AECs, and that inhibition of CARMA3 signaling reduces A. alternata-induced intracellular calcium release. In conclusion, we show that CARMA3 signaling in AECs helps mediate A. alternata-induced allergic airway inflammation, and that CARMA3 is an important signaling molecule for type 2 immune responses in the lung.

Indexed as

AllergensAlternariaAlternariosisAnimalsAsthmaCARD Signaling Adaptor ProteinsCells, CulturedDisease Models, AnimalHumansMicePneumoniaAllergensCARD10 protein, humanCard10 protein, mouseCARD Signaling Adaptor Proteinsallergic lung inflammationasthmaCARMA3

Identifiers

PMID29958012
PMCPMC6293075
OpenAlexW2810149690

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.