Evidence map›Paper›PMID 27456482›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Prostaglandin I2 Suppresses Proinflammatory Chemokine Expression, CD4 T Cell Activation, and STAT6-Independent Allergic Lung Inflammation.

Weisong Zhou, Jian Zhang, Kasia Goleniewska, Daniel E Dulek, Shinji Toki, Dawn C Newcomb, Jacqueline Y Cephus, Robert D Collins, Pingsheng Wu, Mark R Boothby and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Prostaglandin IThe Journal of allergy and clinical immunology · 2025
    Article
  4. Article
  5. A CD4Immunity · 2025
    Article
  6. Can Bisphenols Alter the Inflammation Process?Life (Basel, Switzerland) · 2025
    Review
  7. Prostacyclin synthase deficiency exacerbates systemic inflammatory responses in lipopolysaccharide-induced septic shock in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  8. [Expression of prostacyclin receptor in chronic rhinosinusitis and its relationship with type 2 inflammation].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2024
    Article
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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

11 authors at 1 institution in 1 country.

Weisong ZhouDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and weisong.zhou@vanderbilt.edu.
Jian ZhangDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and.
Kasia GoleniewskaDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and.
Daniel E DulekDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and.
Shinji TokiDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and.ORCID 0000-0003-4379-9118
Dawn C NewcombDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and.
Jacqueline Y CephusDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and.
Robert D CollinsDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232.
Pingsheng WuDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and.
Mark R BoothbyDepartment of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232.
R Stokes PeeblesDivision of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232; and Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232.ORCID 0000-0002-1429-7875
Vanderbilt University · US

Funding

Viral and Host Determinants of Infant and Childhood Allergy and AsthmaU19AI095227 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Dawn C Newcomb · 2011 to 2026
$34.9M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Tissue and Cell Processing CoreU19AI070489 · NIAID · WASHINGTON UNIVERSITY · PI HOLTZMAN, MICHAEL J · 2006 to 2016
$17.9M
Role of Gender in TH17-Mediated Inflammation in Severe AsthmaR01HL122554 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI NEWCOMB, DAWN C · 2015 to 2024
$5.5M
PGI2 regulation of TSLP-mediated allergic inflammation in the lungR01AI111820 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PEEBLES, RAY STOKES · 2014 to 2018
$2.0M
The Role of PGI2 in Allergic InflammationR01HL090664 · NHLBI · VANDERBILT UNIVERSITY · PI PEEBLES, RAY STOKES · 2009 to 2013
$1.9M
The role of ovarian hormones on allergen-mediatedd innate immune airway responsesR21AI121420 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI NEWCOMB, DAWN C · 2016 to 2017
$434k
COX Regulation of Allergic Sensitization and Immune Memory GenerationR56AI076411 · NIAID · VANDERBILT UNIVERSITY · PI ZHOU, WEISONG · 2009 to 2009
$388k
Exogenous PGI2 protection against RSV-induced illnessF30AI118376 · NIAID · VANDERBILT UNIVERSITY · PI BLOODWORTH, MELISSA H. · 2015 to 2019
$152k
The role of cyclooxygenase in the adaptive immune response and toleranceI01BX000624 · VA · VETERANS HEALTH ADMINISTRATION · PI PEEBLES, RAY STOKES · 2009 to 2019
–
BLRD VA I01 BX000624NHLBI NIH HHS R01 HL090664NHLBI NIH HHS R01 HL122554NIAID NIH HHS F30 AI118376NIAID NIH HHS R01 AI111820NIAID NIH HHS R21 AI121420NIAID NIH HHS R56 AI076411NIAID NIH HHS U19 AI070489NIAID NIH HHS U19 AI095227NIGMS NIH HHS T32 GM007347
6 · The paper itself

Abstract

Allergic airway diseases are immune disorders associated with heightened type 2 immune responses and IL-5 and IL-13 production at the site of inflammation. We have previously reported that cyclooxygenase (COX) inhibition by indomethacin augmented allergic airway inflammation in a STAT6-independent manner. However, the key COX product(s) responsible for restraining indomethacin-mediated STAT6-independent allergic inflammation is unknown. In this study, using the mouse model of OVA-induced allergic airway inflammation, we identified that PGI2 receptor (IP) signaling was critical for indomethacin-induced, STAT6-independent proallergic effects. We demonstrated that IP deficiency increased inflammatory cell infiltration, eosinophilia, and IL-5 and IL-13 expression in the lung in a STAT6-independent manner. The augmented STAT6-independent allergic inflammation correlated with enhanced primary immune responses to allergic sensitization and elevated production of multiple inflammatory chemokines (CCL11, CCL17, CCL22, and CXCL12) in the lung after allergen challenge. We also showed that the PGI2 analogue cicaprost inhibited CD4 T cell proliferation and IL-5 and IL-13 expression in vitro, and IP deficiency diminished the stimulatory effect of indomethacin on STAT6-independent IL-5 and IL-13 responses in vivo. The inhibitory effects of PGI2 and the IP signaling pathway on CD4 T cell activation, inflammatory chemokine production, and allergic sensitization and airway inflammation suggest that PGI2 and its analogue iloprost, both Food and Drug Administration-approved drugs, may be useful in treating allergic diseases and asthma. In addition, inhibiting PGI2 signaling by drugs that either block PGI2 production or restrain IP signaling may augment STAT6-independent pathways of allergic inflammation.

Indexed as

AllergensAnimalsAntihypertensive AgentsAsthmaCD4-Positive T-LymphocytesCell ProliferationChemokinesEpoprostenolHypersensitivityIndomethacinInflammationInterleukin-13Interleukin-5LungLymphocyte ActivationMiceAllergensAntihypertensive AgentsChemokinescicaprostEpoprostenolIndomethacinInterleukin-13Interleukin-5OvalbuminReceptors, EpoprostenolStat6 protein, mouseSTAT6 Transcription Factor

Identifiers

PMID27456482
PMCPMC4992670
OpenAlexW2492681811

What OpenQuestion holds

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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.