Evidence map›Paper›PMID 26032511›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2015

Correlation of Cigarette Smoke-Induced Pulmonary Inflammation and Emphysema in C3H and C57Bl/6 Mice.

Elias G Awji, Jean Clare Seagrave, Yohannes Tesfaigzi

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. 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
2.2field-weighted citation impact, top 12% 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. Review
  2. Article
  3. Persistence of emphysema following cessation of cigarette smoke exposure requires a susceptibility factor.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  4. Article
  5. Article
  6. Journal of medical imaging (Bellingham, Wash.) · 2023
    Article
  7. Cigarette smoke-induced airspace disease in mice develops independently of HIF-1α signaling in leukocytes.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

3 authors at 1 institution in 1 country.

Elias G AwjiCOPD Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108.
Jean Clare SeagraveCOPD Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108.
Yohannes TesfaigziCOPD Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108 ytesfaig@lrri.org.
Lovelace Respiratory Research Institute · US

Funding

Resolution of Epithelial Cell Hyperplasia in AsthmaR01HL068111 · NHLBI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI TESFAIGZI, YOHANNES · 2003 to 2021
$10.9M
Resolution of Epithelial Cell HyperplasiaR01ES015482 · NIEHS · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI TESFAIGZI, YOHANNES · 2009 to 2013
$2.6M
Regulation of Mucous Cell Metaplasia in AsthmaR56HL068111 · NHLBI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI TESFAIGZI, YOHANNES · 2007 to 2007
$500k
NHLBI NIH HHS HL68111NIEHS NIH HHS ES015482
6 · The paper itself

Abstract

Cigarette smoke (CS)-exposed mice have been used to model airway inflammation and emphesema in humans; however, the impact of exposure duration, sex, and strain differences in susceptibility to progression of airway inflammation and to emphesema are poorly investigated. This study was designed to determine the association between inflammation and emphysema by exposing 2 strains of mice, C3H/HeN (C3H) and C57BL/6 (Bl/6), to filtered air (FA) or CS for 10, 16, or 22 weeks. Both genders and strains of CS-exposed mice developed pulmonary inflammation as characterized by cell counts in the bronchoalveolar lavage fluid (BALF) and the levels of matrix metalloproteinases (MMPs) in the BALF. CS exposure caused persistently higher number of BALF macrophages in C3H compared to BL/6 mice, while more BALF neutrophils and persistently higher MMP-2 and MMP-9 levels were observed in BL/6 mice. The mean linear intercept (Lm) increased progressively by 26%, 33%, and 55% at 10, 16, and 22 weeks, respectively, in CS-exposed C3H mice compared to the matched air controls. In BL/6 mice, although CS exposure also increased the Lm compared to FA controls, no further increase in Lm beyond the levels observed at 16 weeks of exposure was observed by 22 weeks. These findings suggest that extent of inflammation is not associated with severity of emphysema and underscores the importance of carefully selecting the mouse strains and endpoints when exploring effective treatments for emphesema.

Indexed as

Tobacco ProductsAnimalsBronchoalveolar Lavage FluidCell CountFemaleMaleMatrix MetalloproteinasesMiceMice, Inbred C3HMice, Inbred C57BLNeutrophilsPneumoniaPulmonary AlveoliPulmonary EmphysemaSex CharacteristicsSmokeMatrix MetalloproteinasesSmokealveolar destructioncigarette smokemetalloproteasemouse strains

Identifiers

PMID26032511
PMCPMC4830240
OpenAlexW2302864511

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.