Role of Macrophages in Air Pollution Exposure Related Asthma

Li, Chung-Hsiang; Tsai, Mei-Lan; Chiou, Hsin-Ying Clair; Lin, Yi; Liao, Wei‐Ting; Hung, Chih‐Hsing

doi:10.3390/ijms232012337

Cited by 16 publications

(6 citation statements)

References 123 publications

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“…It has a suppressive effect on Treg cells that may lead to an upsurge of the immune response and thus potentiate the inflammation detected in the lungs of asthmatic subjects (Jaén et al, 2022). It is also found in increased amounts in the serum, exhaled breath, and sputum of COPD subjects, predominantly during disease severity (Li et al, 2022). Raised IL-6 levels were also observed in our study in asthmatic subjects with PCC.…”

Section: Discussionsupporting

confidence: 68%

“…The increased levels of IL-6 in plasma, bronchoalveolar lavage fluid, and sputum of asthmatic subjects have been documented (Mettelman et al, 2022). IL-6 exerts its pro-inflammatory effect in asthma by promoting the differentiation of Th2 and Th17 cells (Li et al, 2022). It has a suppressive effect on Treg cells that may lead to an upsurge of the immune response and thus potentiate the inflammation detected in the lungs of asthmatic subjects (Jaén et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

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Interplay of interleukins (IL6, IL10) and 25 hydroxycholecalciferol in asthmatic subjects with chronic post-COVID condition (PCC)

2024

Trop Biomed

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The study aimed to compare and correlate serum levels of IL-6, 10, and 25-hydroxycholecalciferol in individuals with asthma with and without post-COVID condition (PCC). The study was designed to investigate the inflammatory response and serum 25-hydroxycholecalciferol status in asthmatics with and without PCC. A cross-sectional study of 252 subjects (128 asthmatics and 124 non-asthmatic subjects) was carried out. Interleukins and 25-hydroxycholecalciferol levels were estimated on ELISA. The principle findings were that IL-6 and 25-hydroxycholecalciferol levels were significantly increased (p<0.001), while IL-10 levels were non-significant in asthmatics with PCC compared to those without PCC. However, 25-hydroxycholecalciferol levels were significantly increased, but no significant change was observed in IL-6, and IL-10 levels in non-asthmatics with and without chronic PCC. A significant positive correlation (r = 0.258) was found between 25-hydroxycholecalciferol and IL-6 but a significant negative correlation (r = -0.227) with IL-10 in asthmatics with PCC. Similarly, a significant negative correlation (r = -0.285) was found between 25-hydroxycholecalciferol and IL-10 but was non-significant with IL-6 in asthmatics without PCC. The correlation of 25-hydroxycholecalciferol with IL-10 was significant (0.683), but IL-6 was non-significant in non-asthmatics with PCC. Multiple regression analysis showed that age, IL-6, gender, and PCC were significantly related in adjusted values to 25-hydroxycholecalciferol. This study sheds light on the complex liaison between 25-hydroxycholecalciferol levels and inflammatory responses in asthmatics, especially those with PCC. The findings suggest that although asthmatics with PCC maintain sufficient levels of 25-hydroxycholecalciferol, they show a substantial increase in the proinflammatory response. This suggests that PCC exacerbates the pro-inflammatory response in asthma. Moreover, the study reveals that asthmatics, whether with or without PCC, display a negative correlation between 25-hydroxycholecalciferol and the anti-inflammatory response. This emphasizes the main influence of asthma on the overall inflammatory response. These findings reveal a complex interplay between vitamin D levels and inflammatory mediators in asthmatic individuals with and without PCC.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Interplay of interleukins (IL6, IL10) and 25 hydroxycholecalciferol in asthmatic subjects with chronic post-COVID condition (PCC)

2024

Trop Biomed

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“…PM is thought to serve as an adjuvant that stimulates persistent allergic inflammation in the respiratory tract synergistically with other known pollutants. Heavy metal exposure is known to alter macrophage-related cytokines and surface markers [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Effect of Air Pollutants on Allergic Inflammation in Structural Cells of the Nasal Mucosa

Park,

Moon,

Yang

et al. 2024

Clin Exp Otorhinolaryngol

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Objectives. Air pollution is an increasing global concern, and its effect on allergic inflammation has attracted the attention of many researchers. Particulate matter (PM) is a major component of ambient air pollution, and heavy metals are the primary toxic constituents of PM. As previous studies on the impact of air pollutants on allergic inflammation did not adequately mimic real-world atmospheric exposure, we developed an experimental model to investigate the effects of aerosolized air pollutants on nasal epithelial cells and fibroblasts.Methods. We collected particulate matter 2.5 (PM2.5) samples from ambient 24-hour air samples obtained in Seoul from August 2020 to August 2022, and then conducted component analysis for metallic constituents. Primary nasal epithelial cells and nasal fibroblasts, obtained and cultured from the turbinate tissues of human participants, were treated with PM2.5. The associations of heavy metals identified from the component analysis with cytokine expression were investigated. A three-dimensional (3D)-hybrid culture model, consisting of co-culture of an air-liquid interface and nasal fibroblast spheroids, was constructed to observe the impact of aerosolized air pollutants.Results. Among the heavy metals, Si was the predominant component of PM2.5, and Zn showed the highest correlation with the concentration of PM2.5 in Seoul. PM2.5, Zn, and Si increased the production of epithelial cell-derived cytokines, and PM2.5 and Zn exhibited similar trends with one another. Exposure of the 3D-hybrid model to aerosolized PM2.5 and Zn resulted in elevated periostin, alpha-smooth muscle actin, and fibronectin expression in fibroblast spheroids, and those without an epithelial barrier exhibited a similar increase in periostin expression.Conclusion. Ambient air pollutants in the form of aerosols increase the expression of allergic inflammatory cytokines in both nasal epithelial cells and fibroblasts. Regulations on air pollution will help reduce the global burden of allergic diseases in the future.

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“…Аллергический контактный дерматит на никель развивается у 10-20 % населения [15]. Повышение в биосредах (сыворотка крови, бронхиальный секрет) концентрации IL-6, IFN-γ и TNF-α, IL-2 отмечено в условиях контаминации никелем [16]. Проникновение никеля в организм через кожу или дыхательную систему вызывает развитие аллергической реакции I типа и IV типа, опосредованной реагинами и аллерген-специфическими Тлимфоцитами [17].…”

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Exposure to airborne nickel and phenol and features of the immune response mediated by E and G immunoglobulins

Zaitseva¹,

Dolgikh²,

Dianova³

2023

Health Risk Analysis

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Ambient air pollution with potentially allergenic technogenic haptens facilitates occurrence of atopic reactions and creates favorable conditions for future development of allergic pathologies in exposed population. The aim of this study was to estimate formation of an IgE-mediated and IgG-mediated specific immune response to low-molecular chemical compounds introduced into the body by inhalation (nickel and phenol used as examples). The test groups were made of children (n = 99) and adults (n = 57) who lived under exposure to airborne nickel and phenol in levels not exceeding maximum permissible ones (up to 0.7 MPL). The reference groups included children (n = 95) and adults (n = 53) who lived on a conventionally clean territory. In the test groups, average daily exposure doses of airborne nickel and phenol varied between 0.7•10-6 and 9.3•10-6 mg/(kg•day) for children and between 3.5•10-6 and 5.0•10-5 mg/(kg•day) for adults (the doses were created by emissions from a non-ferrous metallurgy plant); this was 1.5–3.0 times higher than the same indicators in the reference groups. Levels of IgG specific to nickel were more than two times higher in the exposed groups; the exposed children had elevated levels of IgG specific to phenol in their blood, practically three times higher than in the reference group (р < 0.05). By using logistic regression models, we established a significant probabilistic cause-effect relation between elevated nickel levels in children’s blood and elevated levels of IgE-specific to nickel (R2 = 0.87; F = 468.58; р < 0.05). The assessment of the odds ratio made it possible to verify the relationship between nickel levels in blood and the increase in the level of IgE specific to nickel in children (OR = 8.96; 95% CI = 2.00–40.15) and in adults from the test group (OR = 3.12; 95 % CI = 1.10–9.40). The study results indicate that exposure to low levels of airborne nickel and phenol induces hypersensitivity to technogenic haptens in the exposed children and adults. Its distinctive features are an IgE-mediated reaction to nickel and IgG-mediated reaction to phenol. Hyperproduction of immunoglobulin E specific to nickel as well as IgG-antibodies specific to phenol in the exposed children and adults reflects levels of exposure to airborne nickel and phenol and is a peculiarity of a hyperactive immune response developing in the analyzed children on the test territory.

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Role of Macrophages in Air Pollution Exposure Related Asthma

Cited by 16 publications

References 123 publications

Interplay of interleukins (IL6, IL10) and 25 hydroxycholecalciferol in asthmatic subjects with chronic post-COVID condition (PCC)

Interplay of interleukins (IL6, IL10) and 25 hydroxycholecalciferol in asthmatic subjects with chronic post-COVID condition (PCC)

Effect of Air Pollutants on Allergic Inflammation in Structural Cells of the Nasal Mucosa

Exposure to airborne nickel and phenol and features of the immune response mediated by E and G immunoglobulins

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