Imperative role of particulate matter in innate immunity during RNA virus infection
Abstract
Sensing of pathogens by specialized receptors is the hallmark of the innate immune response. Innate immune response also mounts a defense response against various allergens and pollutants including particulate matter present in the atmosphere. Air pollution has been included as the top threat to global health declared by WHO which aims to cover more than three billion people against health emergencies from 2019-2023. Particulate matter (PM), one of the major components of air pollution, is a significant risk factor for many human diseases and its adverse effects include morbidity and premature deaths throughout the world. Several clinical and epidemiological studies have identified a key link between the PM composition and the prevalence of respiratory and inflammatory disorders. However, the underlying molecular mechanism is not well understood. Here, we investigated the influence of air pollutant, PM10 during RNA virus infections using highly pathogenic avian influenza (HPAI). We thus characterized the transcriptomic profile of lung epithelial cell line, A549 treated with PM10 prior to infection with (HPAI) H5N1 influenza virus, which is known to severely affect the lung and cause respiratory damage. We found that PM10 regulates virus infectivity and enhances overall pathogenic burden in the lung cells. Additionally, the transcriptomic profile highlights the connection of host factors related to various metabolic pathways and immune responses which were dysregulated during virus infection. Overall our findings suggest a strong link between the prevalence of respiratory illness and the air quality.
02 /Specification & Classification
Click any tag to browse matching papersReproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Influenza infected macrophages release viral ribonucleoproteins that shape the local host response
Svenja Fritzlar, Seema S. Lakdawala, … Sarah L. Londrigan·bioRxiv·Dec 4, 2023
- TYPE I INTERFERON-DEPENDENT CELLULAR REMODELING DURING ACUTE PULMONARY MHV INFECTION
S. Grabherr, A. Waltenspuehl, … N. B. Pikor·bioRxiv·Feb 1, 2022
- The role of airborne particles in the epidemiology of clade 2.3.4.4b H5N1 high pathogenicity avian influenza virus in commercial poultry production units
J. James, C. J. Warren, … A. C. Banyard·bioRxiv·Mar 16, 2023
- Hypoxia inducible factors regulate Pneumovirus replication by enhancing innate immune sensing
Jiyeon Ha, Parul Sharma, … Peter A. C. Wing·Proceedings of the National Academy of SciencesPeer-reviewed·Apr 7, 2026
- Rhinovirus reduces the severity of subsequent respiratory viral infections by interferon-dependent and -independent mechanisms
J. T. Van Leuven, A. J. Gonzalez, … T. A. Miura·bioRxiv·Nov 6, 2020
- Fibroblast growth factor-9 expression in airway epithelial cells amplifies the type I interferon response and alters influenza A virus pathogenesis
B. Hiller, Y. Yin, … D. Lenschow·bioRxiv·Dec 22, 2021