Evidence map›Paper›PMID 24204830›Full record

ArticlePloS one2013

Chlamydia pneumoniae infection in mice induces chronic lung inflammation, iBALT formation, and fibrosis.

Madhulika Jupelli, Kenichi Shimada, Norika Chiba, Anatoly Slepenkin, Randa Alsabeh, Heather D Jones, Ellena Peterson, Shuang Chen, Moshe Arditi, Timothy R Crother

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. IL-21/IL-21R Promotes the Pro-Inflammatory Effects of Macrophages duringInternational journal of molecular sciences · 2023
    Article
  9. Article
  10. Review
  11. Article
  12. Role of iBALT in Respiratory Immunity.Current topics in microbiology and immunology · 2020
    Review
  13. Neonatal low respiratory tract chlamydiaRespiratory medicine case reports · 2019
    Article
  14. Autophagy Limits Inflammasome DuringFrontiers in immunology · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. A Zebrafish Model forFrontiers in microbiology · 2016
    Article
  19. Review
  20. 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

10 authors at 3 institutions in 1 country.

Madhulika JupelliDivision of Pediatric Infectious Diseases, Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, California, United States of America.
Kenichi Shimada
Norika Chiba
Anatoly Slepenkin
Randa Alsabeh
Heather D Jones
Ellena Peterson
Shuang Chen
Moshe Arditi
Timothy R Crother
Cedars-Sinai Medical Center · USUniversity of California, Irvine · USUniversity of California, Los Angeles · US

Funding

MOLECULAR PATHOGENESIS OF CHLAMYDIA-INDUCED ATHEROGENESIR01HL066436 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2001 to 2013
$3.6M
Role of Innate Immunity in Pathogenesis of Chlamydia Pneumonia InfectionR01AI067995 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2006 to 2010
$1.9M
Innate Immunity and Host Responses in Pathogenesis of Chlamydia PneumoniaeR56AI067995 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2012 to 2012
$413k
NHLBI NIH HHS HL-66436NHLBI NIH HHS R01 HL066436NIAID NIH HHS AI-067995NIAID NIH HHS R01 AI067995NIAID NIH HHS R56 AI067995
6 · The paper itself

Abstract

Chlamydia pneumoniae (CP) lung infection can induce chronic lung inflammation and is associated with not only acute asthma but also COPD exacerbations. However, in mouse models of CP infection, most studies have investigated specifically the acute phase of the infection and not the longer-term chronic changes in the lungs. We infected C57BL/6 mice with 5 × 10(5) CP intratracheally and monitored inflammation, cellular infiltrates and cytokine levels over time to investigate the chronic inflammatory lung changes. While bacteria numbers declined by day 28, macrophage numbers remained high through day 35. Immune cell clusters were detected as early as day 14 and persisted through day 35, and stained positive for B, T, and follicular dendritic cells, indicating these clusters were inducible bronchus associated lymphoid tissues (iBALTs). Classically activated inflammatory M1 macrophages were the predominant subtype early on while alternatively activated M2 macrophages increased later during infection. Adoptive transfer of M1 but not M2 macrophages intratracheally 1 week after infection resulted in greater lung inflammation, severe fibrosis, and increased numbers of iBALTS 35 days after infection. In summary, we show that CP lung infection in mice induces chronic inflammatory changes including iBALT formations as well as fibrosis. These observations suggest that the M1 macrophages, which are part of the normal response to clear acute C. pneumoniae lung infection, result in an enhanced acute response when present in excess numbers, with greater inflammation, tissue injury, and severe fibrosis.

Indexed as

Adoptive TransferAnimalsBacterial LoadB-LymphocytesCell CountChlamydia InfectionsChlamydial PneumoniaChlamydophila pneumoniaeChronic DiseaseCytokinesDendritic CellsFibrosisLungMacrophagesMiceMice, Inbred C57BLCytokines

Identifiers

PMID24204830
PMCPMC3808399
OpenAlexW2061947936

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.