Evidence map›Paper›PMID 28577134›Full record

ArticleInflammation2017

Role of Oxidative Stress in the Suppression of Immune Responses in Peripheral Blood Mononuclear Cells Exposed to Combustible Tobacco Product Preparation.

Subhashini Arimilli, Eckhardt Schmidt, Brad E Damratoski, G L Prasad

Open access · hybridAbstract read
In one paragraph

Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Cigarette smoke and e-cigarette aerosol extracts induce myelopoiesis and suppress inflammatory cytokine production.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  2. HIV-HPV interactions via extracellular vesicles among tobacco smokers and nonsmokers.Experimental biology and medicine (Maywood, N.J.) · 2025
    Article
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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

4 authors at 2 institutions in 1 country.

Subhashini ArimilliDepartment of Microbiology & Immunology, Wake Forest University Health Sciences, Room 2N-052, 575 Patterson Avenue, Winston-Salem, NC, 27101, USA. sarimill@wakehealth.edu.ORCID http://orcid.org/0000-0003-1219-5100
Eckhardt SchmidtRAI Services Company, Winston-Salem, NC, USA.
Brad E DamratoskiDepartment of Regenerative Medicine, Wake Forest University Health Sciences, Winston-Salem, NC, USA.
G L PrasadRAI Services Company, Winston-Salem, NC, USA.
Research Applications (United States) · USWake Forest University · US

Funding

RAI Services Company 100300-660969
6 · The paper itself

Abstract

Cigarette smoking is a major risk factor for several human diseases. Chronic inflammation, resulting from increased oxidative stress, has been suggested as a mechanism that contributes to the increased susceptibility of smokers to cancer and microbial infections. We have previously shown that whole-smoke conditioned medium (WS-CM) and total particulate matter (TPM) prepared from Kentucky 3R4F reference cigarettes [collectively called as combustible tobacco product preparations (TPPs)] potently suppressed agonist-stimulated cytokine secretion and target cell killing in peripheral blood mononuclear cells (PBMCs). Here we have investigated the role of oxidative stress from TPPs, which alters inflammatory responses in vitro. Particularly, we investigated the mechanisms of WS-CM-induced suppression of select cytokine secretions in Toll-like receptor (TLR) agonist-stimulated cells and target cell killing by effector cells in PBMCs. Pretreatment with N-acetyl cysteine (NAC), a precursor of reduced glutathione and an established anti-oxidant, protected against DNA damage and cytotoxicity caused by exposure to WS-CM. Similarly, secretion of tumor necrosis factor (TNF), interleukin (IL)-6, and IL-8 in response to TLR-4 stimulation was restored by pretreatment with NAC. Target cell killing, a functional measure of cytolytic cells in PBMCs, is suppressed by WS-CM. Pretreatment with NAC restored the target cell killing in WS-CM treated PBMCs. This was accompanied by higher perforin levels in the effector cell populations. Collectively, these data suggest that reducing oxidative stress caused by cigarette smoke components restores select immune responses in this ex vivo model.

Indexed as

AcetylcysteineCells, CulturedCytokinesHumansImmunityLeukocytes, MononuclearOxidative StressT-Lymphocytes, CytotoxicTobacco ProductsAcetylcysteineCytokinescytokinescytolysiscytotoxicityLPSN-acetylcysteinePBMCstobacco product preparations

Identifiers

PMID28577134
PMCPMC5587635
OpenAlexW2621199203

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.