Evidence map›Paper›PMID 20160043›Full record

ArticleAmerican journal of respiratory cell and molecular biology2011

Cigarette smoke synergizes lipopolysaccharide-induced interleukin-1β and tumor necrosis factor-α secretion from macrophages via substance P-mediated nuclear factor-κB activation.

Junyang Xu, Fadi Xu, Yong Lin

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. FSTL-1 Attenuation Causes Spontaneous Smoke-Resistant Pulmonary Emphysema.American journal of respiratory and critical care medicine · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Role of NFkB in Drug Addiction: Beyond Inflammation.Alcohol and alcoholism (Oxford, Oxfordshire) · 2017
    Review
  14. Review
  15. Article
  16. Article
  17. Autophagy: a core cellular process with emerging links to pulmonary disease.American journal of respiratory and critical care medicine · 2011
    Review
  18. 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.

Junyang XuLovelace Respiratory Research Institute, Albuquerque, NM 87108, USA.
Fadi Xu
Yong Lin
Lovelace Respiratory Research Institute · US

Funding

Central Mechanisms of Respiratory ArrestR01HL074183 · NHLBI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI XU, FADI · 2004 to 2007
$1.5M
NHLBI NIH HHS HL74183
6 · The paper itself

Abstract

A recent study has indicated that alveolar macrophages from smokers incubated with lipopolysaccharide (LPS) secrete much more IL-1β and TNF-α than those from healthy nonsmokers, but the mechanisms underlying this augmented secretion by cigarette smoke (CS) remain unknown. CS and LPS reportedly promote macrophages' secreting substance P (SP) that could up-regulate these cytokines' secretion from macrophages by acting on neurokinin 1 receptor (NK1R). Moreover, NF-κB from macrophages participates in NK1R intracellular signaling and synthesis of these cytokines. The present in vitro study was undertaken to examine whether CS is able to synergize these cytokines' response to LPS in macrophages, and if so, whether an amplified SP secretion is responsible for this synergistic cytokines' response via a NK1R-driven NF-κB pathway. THP-1-derived and MH-S macrophages were exposed to control medium and CS condensate (CSC) without or with LPS. We found that LPS, CSC, and CSC+LPS significantly increased IL-1β, TNF-α, and SP secretion and that SP secretion markedly preceded cytokines' secretion. CSC+LPS-induced responses were markedly greater than the sum of the responses to CSC and LPS alone, suggesting a synergistic effect. Blocking NK1R reduced the responses of IL-1β, TNF-α, and NF-κB activation to CSC+LPS by 41, 40, and 46%, respectively. NF-κB inhibitors decreased the CSC+LPS-induced cytokines' responses by 70%. Our findings suggest that CS amplifies the LPS-induced macrophages' secretion of IL-1β and TNF-α through synergizing SP secretion, which activates NF-κB via binding with NK1R.

Indexed as

Cell LineCell NucleusEmphysemaHumansInterleukin-1betaLipopolysaccharidesMacrophagesMonocytesNF-kappa BSignal TransductionSmokingSubstance PTumor Necrosis Factor-alphaInterleukin-1betaLipopolysaccharidesNF-kappa BSubstance PTumor Necrosis Factor-alpha

Identifiers

PMID20160043
PMCPMC3095931
OpenAlexW2150839127

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.