How Do Inflammatory Mediators, Immune Response and Air Pollution Contribute to COVID-19 Disease Severity? A Lesson to Learn.
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ABSTRACT:
SUBMITTER: Signorini C
PROVIDER: S-EPMC7996623 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Several epidemiological studies have reported conflicting results on the effect of traffic-related pollutants on markers of inflammation. In a Bayesian framework, we examined the effect of traffic pollution on inflammation using structural equation models (SEMs). We studied measurements of C-reactive protein (CRP), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble intracellular adhesion molecule-1 (sICAM-1) for 749 elderly men from the Normative Aging Study. Using repeated measures SEMs, we fit a latent variable for traffic pollution that is reflected by levels of black carbon, carbon monoxide, nitrogen monoxide and nitrogen dioxide to estimate its effect on a latent variable for inflammation that included sICAM-1, sVCAM-1 and CRP. Exposure periods were assessed using 1-, 2-, 3-, 7-, 14- and 30-day moving averages previsit. We compared our findings using SEMs with those obtained using linear mixed models. Traffic pollution was related to increased inflammation for 3-, 7-, 14- and 30-day exposure periods. An inter-quartile range increase in traffic pollution was associated with a 2.3% (95% posterior interval (PI): 0.0-4.7%) increase in inflammation for the 3-day moving average, with the most significant association observed for the 30-day moving average (23.9%; 95% PI: 13.9-36.7%). Traffic pollution adversely impacts inflammation in the elderly. SEMs in a Bayesian framework can comprehensively incorporate multiple pollutants and health outcomes simultaneously in air pollution-cardiovascular epidemiological studies.
| S-EPMC4648554 | biostudies-literature
Project description:BACKGROUND/OBJECTIVES: There is evidence that exposure to air pollution affects asthma, but the effect of air pollution on asthma severity has not been addressed. The aim was to assess the relation between asthma severity during the past 12 months and home outdoor concentrations of air pollution. METHODS: Asthma severity over the past 12 months was assessed in two complementary ways among 328 adult asthmatics from the French Epidemiological study on the Genetics and Environment of Asthma (EGEA) examined between 1991 and 1995. The four-class severity score integrated clinical events and type of treatment. The five-level asthma score is based only on the occurrence of symptoms. Nitrogen dioxide (NO(2)), sulphur dioxide (SO(2)) and ozone (O(3)) concentrations were assigned to each residence using two different methods. The first was based on the closest monitor data from 1991 to 1995. The second consisted of spatial models that used geostatistical interpolations and then assigned air pollutants to the geo-coded residences (1998). RESULTS: Higher asthma severity score was significantly related to the 8-hour average of ozone during April-September (O(3)-8 h) and the number of days (O(3)-days) with 8-hour ozone averages above 110 microg.m(-3) (for a 36-day increase, equivalent to the interquartile range, in O(3)-days, odds ratio 2.22 (95% confidence interval 1.61 to 3.07) for one class difference in score). Adjustment for age, sex, smoking habits, occupational exposure, and educational level did not alter results. Asthma severity was unrelated to NO(2). Both exposure assessment methods and severity scores resulted in very similar findings. SO(2) correlated with severity but reached statistical significance only for the model-based assignment of exposure. CONCLUSIONS: The observed associations between asthma severity and air pollution, in particular O(3), support the hypothesis that air pollution at levels far below current standards increases asthma severity.
| S-EPMC2663354 | biostudies-literature
Project description:Exposure to air pollution and other environmental inhalation hazards, such as occupational exposures to dusts and fumes, aeroallergens, and tobacco smoke, is a significant cause of chronic lung inflammation leading to respiratory disease. It is now recognized that resolution of inflammation is an active process controlled by a novel family of small lipid mediators termed "specialized pro-resolving mediators" or SPMs, derived mainly from dietary omega-3 polyunsaturated fatty acids. Chronic inflammation results from an imbalance between pro-inflammatory and pro-resolution pathways. Research is ongoing to develop SPMs, and the pro-resolution pathway more generally, as a novel therapeutic approach to diseases characterized by chronic inflammation. Here, we will review evidence that the resolution pathway is dysregulated in chronic lung inflammatory diseases, and that SPMs and related molecules have exciting therapeutic potential to reverse or prevent chronic lung inflammation, with a focus on lung inflammation due to inhalation of environmental hazards including urban particulate matter, organic dusts and tobacco smoke.
| S-EPMC6537608 | biostudies-literature
Project description:BackgroundChronic exposure to air pollution may prime the immune system to be reactive, increasing inflammatory responses to immune stimulation and providing a pathway to increased risk for inflammatory diseases, including asthma and cardiovascular disease. Although long-term exposure to ambient air pollution has been associated with increased circulating markers of inflammation, it is unknown whether it also relates to the magnitude of inflammatory response.ObjectivesThe aim of this study was to examine associations between chronic ambient pollution exposures and circulating and stimulated levels of inflammatory mediators in a cohort of healthy adults.MethodsCirculating interleukin (IL)-6, C-reactive protein (CRP) (n=392), and lipopolysaccharide stimulated production of IL-1β, IL-6, and tumor necrosis factor (TNF)-α (n=379) were measured in the Adult Health and Behavior II cohort. Fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 μm (PM2.5)] and constituents [black carbon (BC), and lead (Pb), manganese (Mn), zinc (Zn), and iron (Fe)] were estimated for each residential address using hybrid dispersion land use regression models. Associations between pollutant exposures and inflammatory measures were examined using linear regression; models were adjusted for age, sex, race, education, smoking, body mass index, and month of blood draw.ResultsThere were no significant correlations between circulating and stimulated measures of inflammation. Significant positive associations were found between exposure to PM2.5 and BC with stimulated production of IL-6, IL-1β, and TNF-α. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of IL-1β and TNF-α. No pollutants were associated with circulating IL-6 or CRP levels.DiscussionExposure to PM2.5, BC, Pb, Mn, Fe, and Zn was associated with increased production of inflammatory mediators by stimulated immune cells. In contrast, pollutant exposure was not related to circulating markers of inflammation. These results suggest that chronic exposure to some pollutants may prime immune cells to mount larger inflammatory responses, possibly contributing to increased risk for inflammatory disease. https://doi.org/10.1289/EHP7089.
| S-EPMC8136520 | biostudies-literature
Project description:Rationale: DNA methylation plays a critical role in asthma development, but differences in DNA methylation associated with asthma severity, especially among adults, are less well-defined. Changes in DNA methylation are influenced by exposure to air pollution, which is a risk factor for asthma exacerbation and severity. Here, we examined how DNA methylomic patterns in adult asthmatics differ by asthma severity and exposure to different components of air pollution. Methods: Peripheral blood CD3+ T cells from adult asthmatics in Beijing, China were serially collected from 37 patients (130 samples total) and analyzed for global DNA methylation using the Illumina MethylationEPIC Array. Measurements and Main Results: Significant differences in DNA methylation were noted among subjects with different degrees of asthma severity, as measured by fraction of exhaled nitric oxide, forced expiratory volume, and asthma control test scores. Differences in DNA methylation were annotated to genes that were enriched in pathways related to asthma or T cell function, and included gene ontology categories related to cellular adhesion, developmental pathways, and calcium signaling. Notable genes that were differentially methylated based on asthma severity included RUNX3, several members of the HLA family, PDGFRA, CDH1, CAV1, and NOTCH4. Differences in DNA methylation also varied by exposure to ambient air pollution, with different components of pollution effecting methylation of different groups of genes. Conclusion: These findings demonstrate how adult asthmatics possess widespread differences in the DNA methylation that associated with varying asthma severity and how air pollution might contribute to more severe asthma via changes in DNA methylation.
2024-07-31 | GSE226257 | GEO
Project description:Dengue virus, a mosquito-borne flavivirus, is a causative agent for dengue infection, which manifests with symptoms ranging from mild fever to fatal dengue shock syndrome. The presence of four serotypes, against which immune cross-protection is short-lived and serotype cross-reactive antibodies that might enhance infection, pose a challenge to further investigate the role of virus and immune response in pathogenesis. We evaluated the viral and immunological factors that correlate with severe dengue disease in a cohort of pediatric dengue patients in New Delhi. Severe dengue disease was observed in both primary and secondary infections. Viral load had no association with disease severity but high viral load correlated with prolonged thrombocytopenia and delayed recovery. Severe dengue cases had low Th1 cytokines and a concurrent increase in the inflammatory mediators such as IL-6, IL-8 and IL-10. A transient increase in CD14+CD16+ intermediate monocytes was observed early in infection. Sorting of monocytes from dengue patient peripheral blood mononuclear cells revealed that it is the CD14+ cells, but not the CD16+ or the T or B cells, that were infected with dengue virus and were major producers of IL-10. Using the Boruta algorithm, reduced interferon-α levels and enhanced aforementioned pro-inflammatory cytokines were identified as some of the distinctive markers of severe dengue. Furthermore, the reduction in the levels of IL-8 and IL-10 were identified as the most significant markers of recovery from severe disease. Our results provide further insights into the immune response of children to primary and secondary dengue infection and help us to understand the complex interplay between the intrinsic factors in dengue pathogenesis.
| S-EPMC4794248 | biostudies-literature
Project description:Rationale: Higher indoor particulate matter (PM) concentrations are linked with increased asthma morbidity. Dietary intake of fatty acids, also linked with asthma outcomes, may influence this relationship. Objectives: To determine the relationship between omega-3 and omega-6 fatty acid intake and pediatric asthma morbidity, and the association between fatty acid intake and strength of indoor, PM-related asthma symptoms, albuterol use, and systemic inflammation. Methods: Analyses included 135 children with asthma enrolled in the AsthmaDIET Study. At baseline, 3 months, and 6 months, data included: week-long average home indoor concentration of PM ≤2.5 μm in aerodynamic diameter and PM ≤10 μm in aerodynamic diameter, dietary intake of omega-3 and omega-6 fatty acids, daily symptoms, and peripheral blood leukocytes. Asthma severity and lung function were assessed at baseline. Multivariable regression models, adjusted for known confounders, were used to determine associations between each fatty acid and outcomes of interest, with interaction terms (fatty acids × PM) in longitudinal analyses. Measurements and Main Results: Higher omega-6 intake associated with increased odds of increased asthma severity (P = 0.02), and lower FEV1/FVC ratio (P = 0.01). Higher omega-3 intake associated with reduced effect of indoor PM ≤2.5 μm in aerodynamic diameter on symptoms (P < 0.01), whereas higher omega-6 intake associated with amplified effect of indoor PM ≤2.5 μm in aerodynamic diameter on symptoms and circulating neutrophil percentage (P < 0.01). Conclusions: Omega-3 and omega-6 intake are associated with pediatric asthma morbidity and may modify the asthmatic response to indoor PM.
| S-EPMC6580674 | biostudies-literature
Project description:Combustion related particulate matter air pollution (PM) is associated with an increased risk of respiratory infections in adults. The exact mechanism underlying this association has not been determined. We hypothesized that increased concentrations of combustion related PM would result in dysregulation of the innate immune system. This epidemiological study includes 111 adult patients hospitalized with respiratory infections who underwent transcriptional analysis of their peripheral blood. We examined the association between gene expression at the time of hospitalization and ambient measurements of particulate air pollutants in the 28 days prior to hospitalization. For each pollutant and time lag, gene-specific linear models adjusting for infection type were fit using LIMMA (Linear Models For Microarray Data), and pathway/gene set analyses were performed using the CAMERA (Correlation Adjusted Mean Rank) program. Comparing patients with viral and/or bacterial infection, the expression patterns associated with air pollution exposure differed. Adjusting for the type of infection, increased concentrations of Delta-C (a marker of biomass smoke) and other PM were associated with upregulation of iron homeostasis and protein folding. Increased concentrations of black carbon (BC) were associated with upregulation of viral related gene pathways and downregulation of pathways related to antigen presentation. The pollutant/pathway associations differed by lag time and by type of infection. This study suggests that the effect of air pollution on the pathogenesis of respiratory infection may be pollutant, timing, and infection specific.
| S-EPMC8484285 | biostudies-literature
Project description: Not available
| S-EPMC5558762 | biostudies-literature
Project description:As our results suggested that metformin acts to limit mitochondrial ROS and calcium-mediated activation of IL-6, we reasoned it would likely affect other processes in alveolar macrophages triggered by exposure to particulate matter (PM). Therefore, we treated mice with metformin in the drinking water for 24 hours before we instilled PM intratracheally. We then flow-sorted alveolar macrophages from whole lung homogenates 24 hours later for transcriptomic analysis (RNA-Seq).
2018-10-05 | GSE98731 | GEO