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Uski, O., Rankin, G. D., Wingfors, H., Magnusson, R., Boman, C., Muala, A., . . . Sandström, T. (2024). In vitro toxicity evaluation in A549 cells of diesel particulate matter from two different particle sampling systems and several resuspension media. Journal of Applied Toxicology
Open this publication in new window or tab >>In vitro toxicity evaluation in A549 cells of diesel particulate matter from two different particle sampling systems and several resuspension media
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2024 (English)In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263Article in journal (Refereed) Epub ahead of print
Abstract [en]

In urban areas, inhalation of fine particles from combustion sources such as diesel engines causes adverse health effects. For toxicity testing, a substantial amount of particulate matter (PM) is needed. Conventional sampling involves collection of PM onto substrates by filtration or inertial impaction. A major drawback to those methodologies is that the extraction process can modify the collected particles and alter their chemical composition. Moreover, prior to toxicity testing, PM samples need to be resuspended, which can alter the PM sample even further. Lastly, the choice of the resuspension medium may also impact the detected toxicological responses. In this study, we compared the toxicity profile of PM obtained from two alternative sampling systems, using in vitro toxicity assays. One system makes use of condensational growth before collection in water in an impinger – BioSampler (CG-BioSampler), and the other, a Dekati® Gravimetric Impactor (DGI), is based on inertial impaction. In addition, various methods for resuspension of DGI collected PM were compared. Tested endpoints included cytotoxicity, formation of cellular reactive oxygen species, and genotoxicity. The alternative collection and suspension methods affected different toxicological endpoints. The water/dimethyl sulfoxide mixture and cell culture medium resuspended particles, along with the CG-BioSampler sample, produced the strongest responses. The water resuspended sample from the DGI appeared least toxic. CG-BioSampler collected PM caused a clear increased response in apoptotic cell death. We conclude that the CG-BioSampler PM sampler is a promising alternative to inertial impaction sampling.

Place, publisher, year, edition, pages
John Wiley & Sons, 2024
Keywords
apoptosis, diesel exhaust, extraction, impinger, particulate matter, reactive oxygen species, sampling, soot, toxicity
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:umu:diva-224261 (URN)10.1002/jat.4616 (DOI)001214370400001 ()38705171 (PubMedID)2-s2.0-85192155238 (Scopus ID)
Available from: 2024-05-14 Created: 2024-05-14 Last updated: 2024-05-14
Eliasson, G., Janson, C., Johansson, G., Larsson, K., Lindén, A., Löfdahl, C.-G., . . . Sundh, J. (2023). Comorbid conditions as predictors of mortality in severe COPD: an eight-year follow-up cohort study. European Clinical Respiratory Journal, 10(1), Article ID 2181291.
Open this publication in new window or tab >>Comorbid conditions as predictors of mortality in severe COPD: an eight-year follow-up cohort study
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2023 (English)In: European Clinical Respiratory Journal, ISSN 2001-8525, Vol. 10, no 1, article id 2181291Article in journal (Refereed) Published
Abstract [en]

Purpose: Co-morbidities are common in chronic obstructive pulmonary disease (COPD) and are associated with increased morbidity and mortality. The aim of the present study was to explore the prevalence of several comorbid conditions in severe COPD, and to investigate and compare their associations with long-term mortality.

Methods: In May 2011 to March 2012, 241 patients with COPD stage 3 or 4 were included in the study. Information was collected on sex, age, smoking history, weight and height, current pharmacological treatment, number of exacerbations the recent year and comorbid conditions. At December 31st, 2019, mortality data (all-cause and cause specific) were collected from the National Cause of Death Register. Data were analyzed using Cox-regression analysis with gender, age, previously established predictors of mortality and comorbid conditions as independent variables, and all-cause mortality and cardiac and respiratory mortality, respectively, as dependent variables.

Results: Out of 241 patients, 155 (64%) were deceased at the end of the study period; 103 patients (66%) died of respiratory disease and 25 (16%) of cardiovascular disease. Impaired kidney function was the only comorbid condition independently associated with increased all-cause mortality (HR (95% CI) 3.41 (1.47-7.93) p=0.004) and respiratory mortality (HR (95%CI) 4.63 (1.61 to 13.4), p = 0.005). In addition, age ≥70, BMI <22 and lower FEV1 expressed as %predicted were significantly associated with increased all-cause and respiratory mortality.

Conclusion: In addition to the risk factors high age, low BMI and poor lung function; impaired kidney function appears to be an important risk factor for mortality in the long term, which should be taken into account in the medical care of patients with severe COPD.

Place, publisher, year, edition, pages
Taylor & Francis, 2023
Keywords
comorbidity, COPD, impaired kidney function, mortality, predictor
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-205729 (URN)10.1080/20018525.2023.2181291 (DOI)000939762500001 ()36861117 (PubMedID)2-s2.0-85149373938 (Scopus ID)
Available from: 2023-03-17 Created: 2023-03-17 Last updated: 2023-03-17Bibliographically approved
Rahman, M., Upadhyay, S., Ganguly, K., Introna, M., Ji, J., Boman, C., . . . Palmberg, L. (2023). Comparable response following exposure to biodiesel and diesel exhaust particles in advanced multicellular human lung models. Toxics, 11(6), Article ID 532.
Open this publication in new window or tab >>Comparable response following exposure to biodiesel and diesel exhaust particles in advanced multicellular human lung models
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2023 (English)In: Toxics, E-ISSN 2305-6304, Vol. 11, no 6, article id 532Article in journal (Refereed) Published
Abstract [en]

Biodiesel is considered to be a sustainable alternative for fossil fuels such as petroleum-based diesel. However, we still lack knowledge about the impact of biodiesel emissions on humans, as airways and lungs are the primary target organs of inhaled toxicants. This study investigated the effect of exhaust particles from well-characterized rapeseed methyl ester (RME) biodiesel exhaust particles (BDEP) and petro-diesel exhaust particles (DEP) on primary bronchial epithelial cells (PBEC) and macrophages (MQ). The advanced multicellular physiologically relevant bronchial mucosa models were developed using human primary bronchial epithelial cells (PBEC) cultured at air–liquid interface (ALI) in the presence or absence of THP-1 cell-derived macrophages (MQ). The experimental set-up used for BDEP and DEP exposures (18 µg/cm2 and 36 µg/cm2) as well as the corresponding control exposures were PBEC-ALI, MQ-ALI, and PBEC co-cultured with MQ (PBEC-ALI/MQ). Following exposure to both BDEP and DEP, reactive oxygen species as well as the stress protein heat shock protein 60 were upregulated in PBEC-ALI and MQ-ALI. Expression of both pro-inflammatory (M1: CD86) and repair (M2: CD206) macrophage polarization markers was increased in MQ-ALI after both BDEP and DEP exposures. Phagocytosis activity of MQ and the phagocytosis receptors CD35 and CD64 were downregulated, whereas CD36 was upregulated in MQ-ALI. Increased transcript and secreted protein levels of CXCL8, as well as IL-6 and TNF-α, were detected following both BDEP and DEP exposure at both doses in PBEC-ALI. Furthermore, the cyclooxygenase-2 (COX-2) pathway, COX-2-mediated histone phosphorylation and DNA damage were all increased in PBEC-ALI following exposure to both doses of BDEP and DEP. Valdecoxib, a COX-2 inhibitor, reduced the level of prostaglandin E2, histone phosphorylation, and DNA damage in PBEC-ALI following exposure to both concentrations of BDEP and DEP. Using physiologically relevant multicellular human lung mucosa models with human primary bronchial epithelial cells and macrophages, we found BDEP and DEP to induce comparable levels of oxidative stress, inflammatory response, and impairment of phagocytosis. The use of a renewable carbon-neutral biodiesel fuel does not appear to be more favorable than conventional petroleum-based alternative, as regards of its potential for adverse health effects.

Place, publisher, year, edition, pages
MDPI, 2023
Keywords
biodiesel, COX-2, DNA damage, lung, MQ-ALI, oxidative stress, particles, PBEC-ALI, petro-diesel, PGE2, phagocytosis
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:umu:diva-212077 (URN)10.3390/toxics11060532 (DOI)001017713500001 ()37368632 (PubMedID)2-s2.0-85163637334 (Scopus ID)
Funder
Swedish Research Council, 2018-03233Swedish Fund for Research Without Animal ExperimentsSwedish Heart Lung Foundation
Available from: 2023-07-17 Created: 2023-07-17 Last updated: 2023-07-17Bibliographically approved
Friberg, M., Behndig, A. F., Bosson, J., Muala, A., Barath, S., Dove, R., . . . Pourazar, J. (2023). Human exposure to diesel exhaust induces CYP1A1 expression and AhR activation without a coordinated antioxidant response. Particle and Fibre Toxicology, 20(1), Article ID 47.
Open this publication in new window or tab >>Human exposure to diesel exhaust induces CYP1A1 expression and AhR activation without a coordinated antioxidant response
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2023 (English)In: Particle and Fibre Toxicology, E-ISSN 1743-8977, Vol. 20, no 1, article id 47Article in journal (Refereed) Published
Abstract [en]

Background: Diesel exhaust (DE) induces neutrophilia and lymphocytosis in experimentally exposed humans. These responses occur in parallel to nuclear migration of NF-κB and c-Jun, activation of mitogen activated protein kinases and increased production of inflammatory mediators. There remains uncertainty regarding the impact of DE on endogenous antioxidant and xenobiotic defences, mediated by nuclear factor erythroid 2-related factor 2 (Nrf2) and the aryl hydrocarbon receptor (AhR) respectively, and the extent to which cellular antioxidant adaptations protect against the adverse effects of DE.

Methods: Using immunohistochemistry we investigated the nuclear localization of Nrf2 and AhR in the epithelium of endobronchial mucosal biopsies from healthy subjects six-hours post exposure to DE (PM10, 300 µg/m3) versus post-filtered air in a randomized double blind study, as a marker of activation. Cytoplasmic expression of cytochrome P450s, family 1, subfamily A, polypeptide 1 (CYP1A1) and subfamily B, Polypeptide 1 (CYP1B1) were examined to confirm AhR activation; with the expression of aldo–keto reductases (AKR1A1, AKR1C1 and AKR1C3), epoxide hydrolase and NAD(P)H dehydrogenase quinone 1 (NQO1) also quantified. Inflammatory and oxidative stress markers were examined to contextualize the responses observed.

Results: DE exposure caused an influx of neutrophils to the bronchial airway surface (p = 0.013), as well as increased bronchial submucosal neutrophil (p < 0.001), lymphocyte (p = 0.007) and mast cell (p = 0.002) numbers. In addition, DE exposure enhanced the nuclear translocation of the AhR and increased the CYP1A1 expression in the bronchial epithelium (p = 0.001 and p = 0.028, respectively). Nuclear translocation of AhR was also increased in the submucosal leukocytes (p < 0.001). Epithelial nuclear AhR expression was negatively associated with bronchial submucosal CD3 numbers post DE (r = −0.706, p = 0.002). In contrast, DE did not increase nuclear translocation of Nrf2 and was associated with decreased NQO1 in bronchial epithelial cells (p = 0.02), without affecting CYP1B1, aldo–keto reductases, or epoxide hydrolase protein expression.

Conclusion: These in vivo human data confirm earlier cell and animal-based observations of the induction of the AhR and CYP1A1 by diesel exhaust. The induction of phase I xenobiotic response occurred in the absence of the induction of antioxidant or phase II xenobiotic defences at the investigated time point 6 h post-exposures. This suggests DE-associated compounds, such as polycyclic aromatic hydrocarbons (PAHs), may induce acute inflammation and alter detoxification enzymes without concomitant protective cellular adaptations in human airways.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2023
Keywords
Aryl hydrocarbon receptor, Diesel exhaust, Immunohistochemistry, Oxidative stress, Xenobiotic metabolism
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:umu:diva-218128 (URN)10.1186/s12989-023-00559-1 (DOI)38062420 (PubMedID)2-s2.0-85178874563 (Scopus ID)
Funder
Västerbotten County CouncilSwedish Heart Lung FoundationUmeå University
Available from: 2023-12-15 Created: 2023-12-15 Last updated: 2023-12-15Bibliographically approved
Hansson, A., Rankin, G., Uski, O., Sehlstedt, M., Pourazar, J., Lindgren, R., . . . Muala, A. (2023). Reduced bronchoalveolar macrophage phagocytosis and cytotoxic effects after controlled short-term exposure to wood smoke in healthy humans. Particle and Fibre Toxicology, 20(1), Article ID 30.
Open this publication in new window or tab >>Reduced bronchoalveolar macrophage phagocytosis and cytotoxic effects after controlled short-term exposure to wood smoke in healthy humans
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2023 (English)In: Particle and Fibre Toxicology, E-ISSN 1743-8977, Vol. 20, no 1, article id 30Article in journal (Refereed) Published
Abstract [en]

Background: Exposure to wood smoke has been shown to contribute to adverse respiratory health effects including airway infections, but the underlying mechanisms are unclear. A preceding study failed to confirm any acute inflammation or cell influx in bronchial wash (BW) or bronchoalveolar lavage (BAL) 24 h after wood smoke exposure but showed unexpected reductions in leukocyte numbers. The present study was performed to investigate responses at an earlier phase, regarding potential development of acute inflammation, as well as indications of cytotoxicity.

Methods: In a double-blind, randomised crossover study, 14 healthy participants were exposed for 2 h to filtered air and diluted wood smoke from incomplete wood log combustion in a common wood stove with a mean particulate matter concentration of 409 µg/m3. Bronchoscopy with BW and BAL was performed 6 h after exposure. Differential cell counts, assessment of DNA-damage and ex vivo analysis of phagocytic function of phagocytosing BAL cells were performed. Wood smoke particles were also collected for in vitro toxicological analyses using bronchial epithelial cells (BEAS-2B) and alveolar type II-like cells (A549).

Results: Exposure to wood smoke increased BAL lactate dehydrogenase (LDH) (p = 0.04) and reduced the ex vivo alveolar macrophage phagocytic capacity (p = 0.03) and viability (p = 0.02) vs. filtered air. BAL eosinophil numbers were increased after wood smoke (p = 0.02), while other cell types were unaffected in BW and BAL. In vitro exposure to wood smoke particles confirmed increased DNA-damage, decreased metabolic activity and cell cycle disturbances.

Conclusions: Exposure to wood smoke from incomplete combustion did not induce any acute airway inflammatory cell influx at 6 h, apart from eosinophils. However, there were indications of a cytotoxic reaction with increased LDH, reduced cell viability and impaired alveolar macrophage phagocytic capacity. These findings are in accordance with earlier bronchoscopy findings at 24 h and may provide evidence for the increased susceptibility to infections by biomass smoke exposure, reported in population-based studies.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2023
Keywords
Air pollution, Biomass combustion, Bronchoscopy, Controlled human exposure, Cytotoxicity, In vitro, Macrophages, Phagocytosis, Wood smoke
National Category
Respiratory Medicine and Allergy Dermatology and Venereal Diseases
Identifiers
urn:nbn:se:umu:diva-212714 (URN)10.1186/s12989-023-00541-x (DOI)37517998 (PubMedID)2-s2.0-85165871931 (Scopus ID)
Funder
Swedish Heart Lung FoundationVästerbotten County CouncilSwedish Energy AgencyUmeå University
Available from: 2023-08-15 Created: 2023-08-15 Last updated: 2023-08-15Bibliographically approved
von Bülow, A., Hansen, S., Sandin, P., Ernstsson, O., Janson, C., Lehtimäki, L., . . . Porsbjerg, C. (2023). Severe asthma trajectories in adults: findings from the NORDSTAR cohort. European Respiratory Journal, 62(3), Article ID 2202474.
Open this publication in new window or tab >>Severe asthma trajectories in adults: findings from the NORDSTAR cohort
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2023 (English)In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 62, no 3, article id 2202474Article in journal (Refereed) Published
Abstract [en]

Background: There is limited evidence on the pathways leading to severe asthma and we are presently unable to effectively predict the progression of the disease. We aimed to describe the longitudinal trajectories leading to severe asthma and to describe clinical events preceding disease progression in a nationwide population of patients with severe asthma.

Methods: We conducted an observational study based on Swedish data from the NORdic Dataset for aSThmA Research (NORDSTAR) research collaboration platform. We identified adult patients with severe asthma in 2018 according to the European Respiratory Society/American Thoracic Society definition and used latent class analysis to identify trajectories of asthma severity over a 10-year retrospective period from 2018.

Results: Among 169 128 asthma patients, we identified 4543 severe asthma patients. We identified four trajectories of severe asthma that were labelled as: trajectory 1 "consistently severe asthma" (n=389 (8.6%)), trajectory 2 "gradual onset severe asthma" (n=942 (20.7%)), trajectory 3 "intermittent severe asthma" (n=1685 (37.1%)) and trajectory 4 "sudden onset severe asthma" (n=1527 (33.6%)). "Consistently severe asthma" had a higher daily inhaled corticosteroid dose and more prevalent osteoporosis compared with the other trajectories. Patients with "gradual onset severe asthma" and "sudden onset severe asthma" developed type 2-related comorbidities concomitantly with development of severe asthma. In the latter group, this primarily occurred within 1-3 years preceding onset of severe asthma.

Conclusions: Four distinct trajectories of severe asthma were identified illustrating different patterns of progression of asthma severity. This may eventually enable the development of better preventive management strategies in severe asthma.

Place, publisher, year, edition, pages
European Respiratory Society, 2023
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-214516 (URN)10.1183/13993003.02474-2022 (DOI)37620041 (PubMedID)2-s2.0-85170581634 (Scopus ID)
Available from: 2023-09-25 Created: 2023-09-25 Last updated: 2023-09-25Bibliographically approved
Brandsma, J., Schofield, J. P. .., Yang, X., Strazzeri, F., Barber, C., Goss, V. M., . . . Djukanović, R. (2023). Stratification of asthma by lipidomic profiling of induced sputum supernatant. Journal of Allergy and Clinical Immunology, 152(1), 117-125
Open this publication in new window or tab >>Stratification of asthma by lipidomic profiling of induced sputum supernatant
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2023 (English)In: Journal of Allergy and Clinical Immunology, ISSN 0091-6749, E-ISSN 1097-6825, Vol. 152, no 1, p. 117-125Article in journal (Refereed) Published
Abstract [en]

Background: Asthma is a chronic respiratory disease with significant heterogeneity in its clinical presentation and pathobiology. There is need for improved understanding of respiratory lipid metabolism in asthma patients and its relation to observable clinical features.

Objective: We performed a comprehensive, prospective, cross-sectional analysis of the lipid composition of induced sputum supernatant obtained from asthma patients with a range of disease severities, as well as from healthy controls.

Methods: Induced sputum supernatant was collected from 211 adults with asthma and 41 healthy individuals enrolled onto the U-BIOPRED (Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes) study. Sputum lipidomes were characterized by semiquantitative shotgun mass spectrometry and clustered using topologic data analysis to identify lipid phenotypes.

Results: Shotgun lipidomics of induced sputum supernatant revealed a spectrum of 9 molecular phenotypes, highlighting not just significant differences between the sputum lipidomes of asthma patients and healthy controls, but also within the asthma patient population. Matching clinical, pathobiologic, proteomic, and transcriptomic data helped inform the underlying disease processes. Sputum lipid phenotypes with higher levels of nonendogenous, cell-derived lipids were associated with significantly worse asthma severity, worse lung function, and elevated granulocyte counts.

Conclusion: We propose a novel mechanism of increased lipid loading in the epithelial lining fluid of asthma patients resulting from the secretion of extracellular vesicles by granulocytic inflammatory cells, which could reduce the ability of pulmonary surfactant to lower surface tension in asthmatic small airways, as well as compromise its role as an immune regulator.

Place, publisher, year, edition, pages
Elsevier, 2023
Keywords
Asthma, epithelial lining fluid, extracellular vesicles, granulocytic inflammation, induced sputum, lipidomics, molecular phenotyping, pulmonary surfactant
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-208055 (URN)10.1016/j.jaci.2023.02.032 (DOI)36918039 (PubMedID)2-s2.0-85153035511 (Scopus ID)
Available from: 2023-05-30 Created: 2023-05-30 Last updated: 2023-07-14Bibliographically approved
Hou, R., Ye, G., Cheng, X., Shaw, D. E., Bakke, P. S., Caruso, M., . . . Djukanović, R. (2023). The role of inflammation in anxiety and depression in the European U-BIOPRED asthma cohorts. Brain, behavior, and immunity, 111, 249-258
Open this publication in new window or tab >>The role of inflammation in anxiety and depression in the European U-BIOPRED asthma cohorts
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2023 (English)In: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 111, p. 249-258Article in journal (Refereed) Published
Abstract [en]

Background: Growing evidence indicates high comorbid anxiety and depression in patients with asthma. However, the mechanisms underlying this comorbid condition remain unclear. The aim of this study was to investigate the role of inflammation in comorbid anxiety and depression in three asthma patient cohorts of the Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes (U-BIOPRED) project. Methods: U-BIOPRED was conducted by a European Union consortium of 16 academic institutions in 11 European countries. A subset dataset from subjects with valid anxiety and depression measures and a large blood biomarker dataset were analysed, including 198 non-smoking patients with severe asthma (SAn), 65 smoking patients with severe asthma (SAs), 61 non-smoking patients with mild-to-moderate asthma (MMA), and 20 healthy non-smokers (HC). The Hospital Anxiety and Depression Scale was used to measure anxiety and depression and a series of inflammatory markers were analysed by the SomaScan v3 platform (SomaLogic, Boulder, Colo). ANOVA and the Kruskal-Wallis test were used for multiple-group comparisons as appropriate. Results: There were significant group effects on anxiety and depression among the four cohort groups (p < 0.05). Anxiety and depression of SAn and SAs groups were significantly higher than that of MMA and HC groups (p < 0.05. There were significant differences in serum IL6, MCP1, CCL18, CCL17, IL8, and Eotaxin among the four groups (p < 0.05). Depression was significantly associated with IL6, MCP1, CCL18 level, and CCL17; whereas anxiety was associated with CCL17 only (p < 0.05). Conclusions: The current study suggests that severe asthma patients are associated with higher levels of anxiety and depression, and inflammatory responses may underlie this comorbid condition.

Place, publisher, year, edition, pages
Academic Press, 2023
Keywords
Anxiety, Asthma, Depression, Inflammation, U-BIOPRED
National Category
Respiratory Medicine and Allergy Psychiatry
Identifiers
urn:nbn:se:umu:diva-208256 (URN)10.1016/j.bbi.2023.04.011 (DOI)001007225000001 ()37146653 (PubMedID)2-s2.0-85156109601 (Scopus ID)
Available from: 2023-05-22 Created: 2023-05-22 Last updated: 2023-09-05Bibliographically approved
Abdel-Aziz, M. I., Vijverberg, S. J. .., Neerincx, A. H., Brinkman, P., Wagener, A. H., Riley, J. H., . . . Maitland-Van der Zee, A. H. (2022). A multi-omics approach to delineate sputum microbiome-associated asthma inflammatory phenotypes [Letter to the editor]. European Respiratory Journal, 59(1), Article ID 2102603.
Open this publication in new window or tab >>A multi-omics approach to delineate sputum microbiome-associated asthma inflammatory phenotypes
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2022 (English)In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 59, no 1, article id 2102603Article in journal, Letter (Refereed) Published
Abstract [en]

A multi-omics approach revealed the underlying biological pathways in the microbiome-driven severe asthma phenotypes. This may help to elucidate new leads for treatment development, particularly for the therapeutically challenging neutrophilic asthma.

Place, publisher, year, edition, pages
European Respiratory Society, 2022
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-192273 (URN)10.1183/13993003.02603-2021 (DOI)000753363000020 ()34824056 (PubMedID)2-s2.0-85123651383 (Scopus ID)
Funder
EU, FP7, Seventh Framework Programme
Available from: 2022-02-11 Created: 2022-02-11 Last updated: 2023-09-05Bibliographically approved
Eklund, L. M., Sköndal, Å., Tufvesson, E., Sjöström, R., Söderström, L., Hanstock, H. G., . . . Stenfors, N. (2022). Cold air exposure at -15 °C induces more airway symptoms and epithelial stress during heavy exercise than rest without aggravated airway constriction. European Journal of Applied Physiology, 122(12), 2533-2544
Open this publication in new window or tab >>Cold air exposure at -15 °C induces more airway symptoms and epithelial stress during heavy exercise than rest without aggravated airway constriction
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2022 (English)In: European Journal of Applied Physiology, ISSN 1439-6319, E-ISSN 1439-6327, Vol. 122, no 12, p. 2533-2544Article in journal (Refereed) Published
Abstract [en]

Purpose: Exposure to cold air may harm the airways. It is unclear to what extent heavy exercise adds to the cold-induced effects on peripheral airways, airway epithelium, and systemic immunity among healthy individuals. We investigated acute effects of heavy exercise in sub-zero temperatures on the healthy airways.

Methods: Twenty-nine healthy individuals underwent whole body exposures to cold air in an environmental chamber at − 15 °C for 50 min on two occasions; a 35-min exercise protocol consisting of a 5-min warm-up followed by 2 × 15 min of running at 85% of VO2max vs. 50 min at rest. Lung function was measured by impulse oscillometry (IOS) and spirometry before and immediately after exposures. CC16 in plasma and urine, and cytokines in plasma were measured before and 60 min after exposures. Symptoms were surveyed pre-, during and post-trials.

Results: FEV1 decreased after rest (− 0.10 ± 0.03 L, p < 0.001) and after exercise (− 0.06 ± 0.02 L, p = 0.012), with no difference between trials. Exercise in − 15 °C induced greater increases in lung reactance (X5; p = 0.023), plasma CC16 (p < 0.001) as well as plasma IL-8 (p < 0.001), compared to rest. Exercise induced more intense symptoms from the lower airways, whereas rest gave rise to more general symptoms.

Conclusion: Heavy exercise during cold air exposure at − 15 °C induced signs of an airway constriction to a similar extent as rest in the same environment. However, biochemical signs of airway epithelial stress, cytokine responses, and symptoms from the lower airways were more pronounced after the exercise trial.

Place, publisher, year, edition, pages
Springer, 2022
Keywords
Cold temperature, Environmental chamber, Healthy, Physical activity, Respiratory physiology, Respiratory symptoms
National Category
Sport and Fitness Sciences Physiology
Identifiers
urn:nbn:se:umu:diva-199479 (URN)10.1007/s00421-022-05004-3 (DOI)000849169500001 ()36053365 (PubMedID)2-s2.0-85137421253 (Scopus ID)
Funder
Swedish Heart Lung FoundationVisare Norr
Available from: 2022-09-20 Created: 2022-09-20 Last updated: 2023-05-23Bibliographically approved
Projects
Health effects of engineered nanoparticles [2008-1375_Formas]; Umeå UniversityBiodiesel - studies of health risks of the vehicle fuels of tomorrow [2015-00403_Forte]; Umeå UniversityNovel biomarkers for air pollution effects in Alzheimer’s disease (ADAIR) [2019-02231_VR]; Umeå University
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-0174-0882

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