Evidence map›Paper›PMID 19360122›Full record

ArticlePLoS pathogens2009

The NOD/RIP2 pathway is essential for host defenses against Chlamydophila pneumoniae lung infection.

Kenichi Shimada, Shuang Chen, Paul W Dempsey, Rosalinda Sorrentino, Randa Alsabeh, Anatoly V Slepenkin, Ellena Peterson, Terence M Doherty, David Underhill, Timothy R Crother and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
12.2field-weighted citation impact, top 1% 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

94 citing papers in PubMed, 157 citations in OpenAlex.

  1. Infection and immunity · 2026
    Article
  2. Article
  3. Article
  4. The N-terminal domain ofFrontiers in immunology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. NOD-like receptors in asthma.Frontiers in immunology · 2022
    Review
  13. LRRK2 plays essential roles in maintaining lung homeostasis and preventing the development of pulmonary fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

34 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
  • Erratum issued
5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Kenichi ShimadaDivision of Pediatrics, Infectious Diseases, and Immunology, Cedars-Sinai Medical Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Shuang Chen
Paul W Dempsey
Rosalinda Sorrentino
Randa Alsabeh
Anatoly V Slepenkin
Ellena Peterson
Terence M Doherty
David Underhill
Timothy R Crother
Moshe Arditi
Cedars-Sinai Medical Center · USUniversity of California, Los Angeles · USUniversity of California, Irvine · 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 HL66436NHLBI NIH HHS R01 HL066436NIAID NIH HHS AI 067995NIAID NIH HHS R01 AI067995NIAID NIH HHS R56 AI067995
6 · The paper itself

Abstract

Here we investigated the role of the Nod/Rip2 pathway in host responses to Chlamydophila pneumoniae-induced pneumonia in mice. Rip2(-/-) mice infected with C. pneumoniae exhibited impaired iNOS expression and NO production, and delayed neutrophil recruitment to the lungs. Levels of IL-6 and IFN-gamma levels as well as KC and MIP-2 levels in bronchoalveolar lavage fluid (BALF) were significantly decreased in Rip2(-/-) mice compared to wild-type (WT) mice at day 3. Rip2(-/-) mice showed significant delay in bacterial clearance from the lungs and developed more severe and chronic lung inflammation that continued even on day 35 and led to increased mortality, whereas WT mice cleared the bacterial load, recovered from acute pneumonia, and survived. Both Nod1(-/-) and Nod2(-/-) mice also showed delayed bacterial clearance, suggesting that C. pneumoniae is recognized by both of these intracellular receptors. Bone marrow chimera experiments demonstrated that Rip2 in BM-derived cells rather than non-hematopoietic stromal cells played a key role in host responses in the lungs and clearance of C. pneumoniae. Furthermore, adoptive transfer of WT macrophages intratracheally was able to rescue the bacterial clearance defect in Rip2(-/-) mice. These results demonstrate that in addition to the TLR/MyD88 pathway, the Nod/Rip2 signaling pathway also plays a significant role in intracellular recognition, innate immune host responses, and ultimately has a decisive impact on clearance of C. pneumoniae from the lungs and survival of the infectious challenge.

Indexed as

Immunity, InnateAnimalsBone Marrow CellsChemokinesChlamydophila InfectionsChlamydophila pneumoniaeEnzyme-Linked Immunosorbent AssayFlow CytometryMacrophagesMiceMice, KnockoutNeutrophil InfiltrationNitric OxideNitric Oxide Synthase Type IINod Signaling Adaptor ProteinsPneumonia, BacterialChemokinesNitric OxideNitric Oxide Synthase Type IINod Signaling Adaptor ProteinsReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesRipk2 protein, mouseRNA, Messenger

Identifiers

PMID19360122
PMCPMC2660273
OpenAlexW2165549236

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.