ArticlePhysiological reports2021
Diesel exposure increases susceptibility of primary human nasal epithelial cells to rhinovirus infection.
Article in Physiological reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- The triple-hit hypothesis: exploring pulmonary e-cigarette, PMEuropean respiratory review : an official journal of the European Respiratory Society · 2026Review
- Impact of air pollution on exacerbations of respiratory and cardiovascular diseases for the intensivist: a narrative review.Intensive care medicine experimental · 2026Review
- 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
- Diesel exposure increases susceptibility of primary human nasal epithelial cells to rhinovirus infection.Physiological reports · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nasal epithelial cells (NECs) are among the first cells to be exposed to air pollutants and respiratory viruses. Although it is known that air pollution exposure and rhinovirus infections increase the risk for asthma development independently, it is unclear how these risk factors interact on a cellular level. Therefore, we aimed to investigate how exposure to diesel particulate matter (DPM) modifies the response of primary NECs to rhinovirus (RV) infection in vitro. Exposure of re-differentiated, primary NECs (49 healthy children [0-7 years], 12 adults) to DPM modified the mRNA expression of viral cell-surface receptors, pattern recognition receptors, and pro-inflammatory response (also protein levels). After exposure to DPM, we additionally infected the NECs with RV-1b and RV-16. Viral loads (assessed by titration assays) were significantly higher in DPM-exposed compared with non-exposed NECs. Exposure to DPM prior to RV infection resulted in a significant upregulation of pro-inflammatory cytokines (mRNA and protein level) and β-defensins mRNA, and significant downregulation of pattern recognition receptors mRNA and CXCL10 (mRNA and protein levels). There was no difference between all outcomes of NECs from children and adults. We can conclude that exposure to DPM prior to RV infection increases viral loads by downregulation of viral defense receptors and upregulation of pro-inflammatory cytokines. Our findings indicate a strong interaction between air pollution and the antiviral response to RV infection in NECs. We provide mechanistic evidence that exposure to air pollution increases susceptibility to RV infection.
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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.