ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Suppression of the NF-κB pathway by diesel exhaust particles impairs human antimycobacterial immunity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 citations in OpenAlex.
- A systematic review and meta-analysis on the association between ambient air pollution and pulmonary tuberculosis.Scientific reports · 2022Pooled it
- Effects of Air Pollution on Lung Innate Lymphoid Cells: Review of In Vitro and In Vivo Experimental Studies.International journal of environmental research and public health · 2019Pooled it
- Optimal Scale of Greenspace Exposure for Pulmonary Tuberculosis Treatment Success: Multi-scale Associations and Interactions with Air Pollutants.Journal of urban health : bulletin of the New York Academy of Medicine · 2026Article
- The impact of air pollution on active tuberculosis development from latent tuberculosis infection in rural China: 10-year follow-up of a cohort study.ERJ open research · 2025Article
- Machine learning identifies environmental drivers of pulmonary tuberculosis in Xinjiang a typical arid region of China.Scientific reports · 2025Article
- Correlations between human alveolar macrophage particulate matter load, air pollution particulate matter levels, and systemic inflammation markers in Mexico City.Scientific reports · 2025Article
- The association between pulmonary tuberculosis recurrence and exposure to fine particulate matter and residential greenness: A population-based retrospective study.One health (Amsterdam, Netherlands) · 2025Article
- Exposure to Urban Air Pollution Particulate Matter Modifies Th1/Th2American journal of respiratory cell and molecular biology · 2025Article
- A mediation analysis of meteorological factors on the association between ambient carbon monoxide and tuberculosis outpatients visits.Frontiers in public health · 2025Article
- Association between ambient particulate matter and latent tuberculosis infection among 198 275 students.Journal of global health · 2024Article
- Impact of fine particulate matter on latent tuberculosis infection and active tuberculosis in older adults: a population-based multicentre cohort study.Emerging microbes & infections · 2024Article
- Ambient air pollution contributed to pulmonary tuberculosis in China.Emerging microbes & infections · 2024Article
- Association of Fine Particulate Matter and Residential Greenness With Risk of Pulmonary Tuberculosis Retreatment: Population-Based Retrospective Study.JMIR public health and surveillance · 2024Article
- Air Pollution Drives Macrophage Senescence through a Phagolysosome-15-Lipoxygenase Pathway.ImmunoHorizons · 2024Article
- Impact of diesel exhaust particles on infections with Mycobacterium bovis BCG in in vitro human macrophages and an in vivo Galleria mellonella model.Environmental pollution (Barking, Essex : 1987) · 2024Article
- Chemical exposure and alveolar macrophages responses: 'the role of pulmonary defense mechanism in inhalation injuries'.BMJ open respiratory research · 2023Review
- Machine Learning Prediction Model of Tuberculosis Incidence Based on Meteorological Factors and Air Pollutants.International journal of environmental research and public health · 2023Article
- Association of Daily Exposure to Air Pollutants with the Risk of Tuberculosis in Xuhui District of Shanghai, China.International journal of environmental research and public health · 2022Article
- Lagged Effects of Exposure to Air Pollutants on the Risk of Pulmonary Tuberculosis in a Highly Polluted Region.International journal of environmental research and public health · 2022Article
- Association of long-term exposure to ambient air pollution with the number of tuberculosis cases notified: a time-series study in Hong Kong.Environmental science and pollution research international · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiological studies suggest that chronic exposure to air pollution increases susceptibility to respiratory infections, including tuberculosis in humans. A possible link between particulate air pollutant exposure and antimycobacterial immunity has not been explored in human primary immune cells. We hypothesized that exposure to diesel exhaust particles (DEP), a major component of urban fine particulate matter, suppresses antimycobacterial human immune effector cell functions by modulating TLR-signaling pathways and NF-κB activation. We show that DEP and H37Ra, an avirulent laboratory strain of Mycobacterium tuberculosis, were both taken up by the same peripheral human blood monocytes. To examine the effects of DEP on M. tuberculosis-induced production of cytokines, PBMC were stimulated with DEP and M. tuberculosis or purified protein derivative. The production of M. tuberculosis and purified protein derivative-induced IFN-γ, TNF-α, IL-1β, and IL-6 was reduced in a DEP dose-dependent manner. In contrast, the production of anti-inflammatory IL-10 remained unchanged. Furthermore, DEP stimulation prior to M. tuberculosis infection altered the expression of TLR3, -4, -7, and -10 mRNAs and of a subset of M. tuberculosis-induced host genes including inhibition of expression of many NF-κB (e.g., CSF3, IFNG, IFNA, IFNB, IL1A, IL6, and NFKBIA) and IFN regulatory factor (e.g., IFNG, IFNA1, IFNB1, and CXCL10) pathway target genes. We propose that DEP downregulate M. tuberculosis-induced host gene expression via MyD88-dependent (IL6, IL1A, and PTGS2) as well as MyD88-independent (IFNA, IFNB) pathways. Prestimulation of PBMC with DEP suppressed the expression of proinflammatory mediators upon M. tuberculosis infection, inducing a hyporesponsive cellular state. Therefore, DEP alters crucial components of antimycobacterial host immune responses, providing a possible mechanism by which air pollutants alter antimicrobial immunity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.