Evidence map›Paper›PMID 21421908›Full record

ArticleAmerican journal of respiratory cell and molecular biology2011

Blocking the leukotriene B4 receptor 1 inhibits late-phase airway responses in established disease.

Koichi Waseda, Nobuaki Miyahara, Arihiko Kanehiro, Genyo Ikeda, Hikari Koga, Yasuko Fuchimoto, Etsuko Kurimoto, Yasushi Tanimoto, Mikio Kataoka, Mitsune Tanimoto and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-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

8 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Cigarette smoke-induced lung inflammation in COPD mediated via LTB4/BLT1/SOCS1 pathway.International journal of chronic obstructive pulmonary disease · 2016
    Article
  5. Article
  6. Article
  7. Article
  8. Article
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 2 institutions in 2 countries.

Koichi WasedaDepartment of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
Nobuaki Miyahara
Arihiko Kanehiro
Genyo Ikeda
Hikari Koga
Yasuko Fuchimoto
Etsuko Kurimoto
Yasushi Tanimoto
Mikio Kataoka
Mitsune Tanimoto
Erwin W Gelfand
Okayama University · JPNational Jewish Health · US

Funding

Signaling Memory in Chronic AsthmaP01HL036577 · NHLBI · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 1986 to 2011
$18.7M
Naturally Occurring T Regulatory Cells Control Airway HyperresponsivenessR01AI077609 · NIAID · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 2009 to 2013
$2.3M
RSV ENHANCES SENSITIZATION AND AIRWAY RESPONSIVENESSR01HL061005 · NHLBI · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 1999 to 2007
$2.2M
Naturally occurring T regulatory cells control airway hyperresponsivenessR56AI077609 · NIAID · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 2008 to 2008
$487k
NHLBI NIH HHS HL-36577NHLBI NIH HHS HL-61005NHLBI NIH HHS P01 HL036577NHLBI NIH HHS R01 HL061005NIAID NIH HHS AI-77609NIAID NIH HHS R01 AI077609NIAID NIH HHS R56 AI077609
6 · The paper itself

Abstract

Most of the studies investigating the effectiveness of blocking the leukotriene B4 (LTB4) receptor 1 (BLT1) have been performed in models of primary or acute allergen challenge. The role of the LTB4-BLT1 pathway in secondary challenge models, where airway hyperresponsiveness (AHR) and airway inflammation have been established, has not been defined. We investigated the effects of blocking BLT1 on early- and late-phase development of AHR and airway inflammation in previously sensitized and challenged mice. Female BALB/c mice were sensitized (Days 1 and 14) and challenged (primary, Days 28-30) with ovalbumin. On Day 72, mice were challenged (secondary) with a single OVA aerosol, and the early and late phases of AHR and inflammation were determined. Specific blockade of BLT1 was attained by oral administration of a BLT1 antagonist on Days 70 through 72. Administration of the antagonist inhibited the secondary ovalbumin challenge-induced alterations in airway responses during the late phase but not during the early phase, as demonstrated by decreases in AHR and in bronchoalveolar lavage neutrophilia and eosinophilia 6 and 48 hours after secondary challenge. The latter was associated with decreased levels of KC protein, macrophage inflammatory protein 2, and IL-17 in the airways. These data identify the importance of the LTB4-BLT1 pathway in the development of late-phase, allergen-induced airway responsiveness after secondary airway challenge in mice with established airway disease.

Indexed as

AnimalsAnti-Asthmatic AgentsAntibodiesAsthmaBronchial HyperreactivityBronchial Provocation TestsBronchoalveolar Lavage FluidChemokine CXCL1Chemokine CXCL2Disease Models, AnimalFemaleInflammation MediatorsInterleukin-17Leukotriene AntagonistsLungMiceAnti-Asthmatic AgentsAntibodiesChemokine CXCL1Chemokine CXCL2Cxcl1 protein, mouseCxcl2 protein, mouseInflammation MediatorsInterleukin-17Leukotriene AntagonistsLtb4r1 protein, mouseOvalbuminReceptors, Leukotriene B4

Identifiers

PMID21421908
PMCPMC3208610
OpenAlexW1982342687

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.