Evidence map›Paper›PMID 21665963›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011

Organic dust augments nucleotide-binding oligomerization domain expression via an NF-{kappa}B pathway to negatively regulate inflammatory responses.

Jill A Poole, Tammy Kielian, Todd A Wyatt, Angela M Gleason, Jeremy Stone, Kelsey Palm, William W West, Debra J Romberger

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. NOD2-NLRP3 Axis and Asthma.Journal of asthma and allergy · 2025
    Review
  2. Article
  3. Organic dust induces inflammatory gene expression in lung epithelial cells via ROS-dependent STAT-3 activation.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  4. The Effect of Inhalant Organic Dust on Bone Health.Current allergy and asthma reports · 2018
    Review
  5. Article
  6. Review
  7. cAMP-dependent protein kinase activation decreases cytokine release in bronchial epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2014
    Article
  8. Article
  9. Article
  10. CD11c(+)/CD11b(+) cells are critical for organic dust-elicited murine lung inflammation.American journal of respiratory cell and molecular biology · 2012
    Article
  11. αβ T cells and a mixed Th1/Th17 response are important in organic dust-induced airway disease.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2012
    Article
  12. Article
  13. Farming-associated environmental exposures and effect on atopic diseases.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2012
    Review
  14. Role of NOD2 in regulating the immune response to Aspergillus fumigatus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012
    Article
  15. Immunological and inflammatory responses to organic dust in agriculture.Current opinion in allergy and clinical immunology · 2012
    Review
  16. Respiratory health effects of large animal farming environments.Journal of toxicology and environmental health. Part B, Critical reviews · 2012
    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

8 authors at 2 institutions in 1 country.

Jill A PoolePulmonary, Critical Care, Sleep & Allergy Division; Dept. of Medicine, Univ. of Nebraska Medical Center, 985300 The Nebraska Medical Center, Omaha, NE 68198-5300, USA. japoole@unmc.edu
Tammy Kielian
Todd A Wyatt
Angela M Gleason
Jeremy Stone
Kelsey Palm
William W West
Debra J Romberger
Omaha VA Medical Center · USUniversity of Nebraska Medical Center · US

Funding

Role of pattern recognition receptors in organic dust-induced airway inflammationR01ES019325 · NIEHS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI POOLE, JILL A · 2010 to 2020
$3.7M
Airway Injury Caused by MAA AdductsR01AA017993 · NIAAA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WYATT, TODD A · 2008 to 2012
$1.9M
Receptors Involved in Microglial Responses to S. aureusR01NS055385 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI KIELIAN, TAMMY L · 2007 to 2010
$1.1M
Chronic Innate Immune Adaptation to Organic DustK08ES015522 · NIEHS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI POOLE, JILL A · 2007 to 2011
$944k
NIAAA NIH HHS R01 AA017993NIEHS NIH HHS ES015522-03S1NIEHS NIH HHS K08:ES015522-01NIEHS NIH HHS R01 ES019325NIEHS NIH HHS R01: ES019325NINDS NIH HHS R01 NS055385
6 · The paper itself

Abstract

Nucleotide-binding oligomerization domain 2 (NOD2) is involved in innate immune responses to peptidoglycan degradation products. Peptidoglycans are important mediators of organic dust-induced airway diseases in exposed agriculture workers; however, the role of NOD2 in response to complex organic dust is unknown. Monocytes/macrophages were exposed to swine facility organic dust extract (ODE), whereupon NOD2 expression was evaluated by real-time PCR and Western blot. ODE induced significant NOD2 mRNA and protein expression at 24 and 48 h, respectively, which was mediated via a NF-κB signaling pathway as opposed to a TNF-α autocrine/paracrine mechanism. Specifically, NF-κB translocation increased rapidly following ODE stimulation as demonstrated by EMSA, and inhibition of the NF-κB pathway significantly reduced ODE-induced NOD2 expression. However, there was no significant reduction in ODE-induced NOD2 gene expression when TNF-α was inhibited or absent. Next, it was determined whether NOD2 regulated ODE-induced inflammatory cytokine production. Knockdown of NOD2 expression by small interfering RNA resulted in increased CXCL8 and IL-6, but not TNF-α production in response to ODE. Similarly, primary lung macrophages from NOD2 knockout mice demonstrated increased IL-6, CXCL1, and CXCL1, but not TNF-α, expression. Lastly, a higher degree of airway inflammation occurred in the absence of NOD2 following acute (single) and repetitive (3 wk) ODE exposure in an established in vivo murine model. In summary, ODE-induced NOD2 expression is directly dependent on NF-κB signaling, and NOD2 is a negative regulator of complex, organic dust-induced inflammatory cytokine/chemokine production in mononuclear phagocytes.

Indexed as

DustAgricultureAnimalsHumansInflammationInterleukin-6Interleukin-8Macrophages, AlveolarMiceMonocytesNF-kappa BNod2 Signaling Adaptor ProteinRNA, Small InterferingSwineTumor Necrosis Factor-alphaCXCL8 protein, humanDustIL6 protein, humanInterleukin-6Interleukin-8NF-kappa BNod2 Signaling Adaptor ProteinRNA, Small InterferingTumor Necrosis Factor-alpha

Identifiers

PMID21665963
PMCPMC3174739
OpenAlexW2098712124

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.