Evidence map›Paper›PMID 25582403›Full record

ReviewImmunobiology2015

Hyaluronan fragments as mediators of inflammation in allergic pulmonary disease.

Sumit Ghosh, Scott A Hoselton, Glenn P Dorsam, Jane M Schuh

Abstract readReview
In one paragraph

Review in Immunobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Hyaluronan in immune dysregulation and autoimmune diseases.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Modified High-Molecular-Weight Hyaluronan Promotes Allergen-Specific Immune Tolerance.American journal of respiratory cell and molecular biology · 2017
    Article
  10. Review
  11. HYAL-2-WWOX-SMAD4 Signaling in Cell Death and Anticancer Response.Frontiers in cell and developmental biology · 2016
    Review
  12. Review
  13. Article
  14. Article
  15. Cigarette Smoke Particle-Induced Lung Injury and Iron Homeostasis.International journal of chronic obstructive pulmonary disease
    Review
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

4 authors at 1 institution in 1 country.

Sumit GhoshDepartment of Veterinary and Microbiological Sciences, North Dakota State University, Fargo, ND 58108, USA. Electronic address: Sumit.Ghosh@ndsu.edu.
Scott A HoseltonDepartment of Veterinary and Microbiological Sciences, North Dakota State University, Fargo, ND 58108, USA.
Glenn P DorsamDepartment of Veterinary and Microbiological Sciences, North Dakota State University, Fargo, ND 58108, USA.
Jane M SchuhDepartment of Veterinary and Microbiological Sciences, North Dakota State University, Fargo, ND 58108, USA.
North Dakota State University · US

Funding

HA in fungal allergic asthmaR15HL117254 · NHLBI · NORTH DAKOTA STATE UNIVERSITY · PI SCHUH, JANE M · 2013 to 2013
$435k
NHLBI NIH HHS 1R15HL117254-01NHLBI NIH HHS R15 HL117254
6 · The paper itself

Abstract

Asthma is frequently caused and/or exacerbated by sensitization to allergens, which are ubiquitous in many indoor and outdoor environments. Severe asthma is characterized by airway hyperresponsiveness and bronchial constriction in response to an inhaled allergen, leading to a disease course that is often very difficult to treat with standard asthma therapies. As a result of interactions among inflammatory cells, structural cells, and the intercellular matrix of the allergic lung, patients with sensitization to allergens may experience a greater degree of tissue injury followed by airway wall remodeling and progressive, accumulated pulmonary dysfunction as part of the disease sequela. In addition, turnover of extracellular matrix (ECM) components is a hallmark of tissue injury and repair. This review focuses on the role of the glycosaminoglycan hyaluronan (HA), a component of the ECM, in pulmonary injury and repair with an emphasis on allergic asthma. Both the synthesis and degradation of the ECM are critical contributors to tissue repair and remodeling. Fragmented HA accumulates during tissue injury and functions in ways distinct from the larger native polymer. There is gathering evidence that HA degradation products are active participants in stimulating the expression of inflammatory genes in a variety of immune cells at the injury site. In this review, we will consider recent advances in the understanding of the mechanisms that are associated with HA accumulation and inflammatory cell recruitment in the asthmatic lung.

Indexed as

Airway RemodelingAnimalsAsthmaCell MovementExtracellular MatrixHumansHyaluronic AcidInflammation MediatorsLungPeptide FragmentsHyaluronic AcidInflammation MediatorsPeptide FragmentsAsthmaExtracellular matrixHyaluronan

Identifiers

PMID25582403
PMCPMC4393768
OpenAlexW2039356605

What OpenQuestion holds

Textmetadata
LicenceTDM
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.