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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
Åpne denne publikasjonen i ny fane eller vindu >>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 (engelsk)Inngår i: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263Artikkel i tidsskrift (Fagfellevurdert) 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.

sted, utgiver, år, opplag, sider
John Wiley & Sons, 2024
Emneord
apoptosis, diesel exhaust, extraction, impinger, particulate matter, reactive oxygen species, sampling, soot, toxicity
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-224261 (URN)10.1002/jat.4616 (DOI)001214370400001 ()38705171 (PubMedID)2-s2.0-85192155238 (Scopus ID)
Tilgjengelig fra: 2024-05-14 Laget: 2024-05-14 Sist oppdatert: 2024-07-02
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.
Åpne denne publikasjonen i ny fane eller vindu >>Reduced bronchoalveolar macrophage phagocytosis and cytotoxic effects after controlled short-term exposure to wood smoke in healthy humans
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2023 (engelsk)Inngår i: Particle and Fibre Toxicology, E-ISSN 1743-8977, Vol. 20, nr 1, artikkel-id 30Artikkel i tidsskrift (Fagfellevurdert) 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.

sted, utgiver, år, opplag, sider
BioMed Central (BMC), 2023
Emneord
Air pollution, Biomass combustion, Bronchoscopy, Controlled human exposure, Cytotoxicity, In vitro, Macrophages, Phagocytosis, Wood smoke
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-212714 (URN)10.1186/s12989-023-00541-x (DOI)37517998 (PubMedID)2-s2.0-85165871931 (Scopus ID)
Forskningsfinansiär
Swedish Heart Lung FoundationVästerbotten County CouncilSwedish Energy AgencyUmeå University
Tilgjengelig fra: 2023-08-15 Laget: 2023-08-15 Sist oppdatert: 2024-07-02bibliografisk kontrollert
Antoniewicz, L., Kabele, M., Nilsson, U., Pourazar, J., Rankin, G., Bosson, J. A. & Lundbäck, M. (2022). Chronic snus use in healthy males alters endothelial function and increases arterial stiffness. PLOS ONE, 17(6), Article ID e0268746.
Åpne denne publikasjonen i ny fane eller vindu >>Chronic snus use in healthy males alters endothelial function and increases arterial stiffness
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2022 (engelsk)Inngår i: PLOS ONE, E-ISSN 1932-6203, Vol. 17, nr 6, artikkel-id e0268746Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Snus usage is commonly touted as a safer alternative to cigarette smoking. However, recent studies have demonstrated possible adverse cardiovascular effects in chronic snus users. The present study evaluates the effects of chronic snus use on vascular function by assessing central arterial stiffness and endothelial vasodilatory function in healthy chronic snus users as compared to matched non-users.

Methods and results: Fifty healthy males (24 snus users, 26 age-matched controls) with a mean age of 44 years were included in the study. Arterial stiffness was assessed employing both pulse wave velocity and pulse wave analysis. Endothelial vasodilatory function was measured by venous occlusion plethysmography, utilizing intra-arterial administration of acetylcholine, glyceryl trinitrate and bradykinin to further gauge endothelium-dependent and -independent vasodilatory function. Arterial stiffness was significantly higher in chronic snus users as compared to controls: pulse wave velocity [m/s]: 6.6±0.8 vs 7.1±0.9 resp. (p = 0.026), augmentation index corrected for heart rate [%]: 0.1±13.2 vs 7.3±7.8 resp. (p = 0.023). Endothelial independent vasodilation, i.e. the reaction to glyceryl trinitrate, was significantly lower in snus users as measured by venous occlusion plethysmography.

Conclusions: The results of this study show an increased arterial stiffness and an underlying endothelial dysfunction in daily snus users as compared to matched non-tobacco controls. These findings indicate that long-term use of snus may alter the function of the endothelium and therefore reinforces the assertion that chronic snus use is correlated to an increased risk of development of cardiovascular disease.

sted, utgiver, år, opplag, sider
Public Library of Science (PLoS), 2022
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-203175 (URN)10.1371/journal.pone.0268746 (DOI)000832307900135 ()35657943 (PubMedID)2-s2.0-85131702456 (Scopus ID)
Forskningsfinansiär
The Swedish Heart and Lung AssociationVästerbotten County CouncilSwedish Heart Lung FoundationKarolinska InstituteStockholm County CouncilUmeå UniversityMagnus Bergvall FoundationSwedish Society of Medicine
Tilgjengelig fra: 2023-01-16 Laget: 2023-01-16 Sist oppdatert: 2024-04-08bibliografisk kontrollert
Tuiskunen-Bäck, A., Rasmuson, J., Thunberg, T., Rankin, G., Wigren Byström, J., Andersson, C., . . . Ahlm, C. (2022). Clinical and genomic characterisation of a fatal Puumala orthohantavirus case with low levels of neutralising antibodies. Infectious Diseases, 54(10), 766-772
Åpne denne publikasjonen i ny fane eller vindu >>Clinical and genomic characterisation of a fatal Puumala orthohantavirus case with low levels of neutralising antibodies
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2022 (engelsk)Inngår i: Infectious Diseases, ISSN 2374-4235, E-ISSN 2374-4243, Vol. 54, nr 10, s. 766-772Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

BACKGROUND: Orthohantaviruses are rodent-borne emerging viruses that cause haemorrhagic fever with renal syndrome (HFRS) in Eurasia and hantavirus pulmonary syndrome in America. Transmission between humans have been reported and the case-fatality rate ranges from 0.4% to 40% depending on virus strain. There is no specific and efficient treatment for patients with severe HFRS. Here, we characterised a fatal case of HFRS and sequenced the causing Puumala orthohantavirus (PUUV).

METHODS: PUUV RNA and virus specific neutralising antibodies were quantified in plasma samples from the fatal case and other patients with non-fatal PUUV infection. To investigate if the causing PUUV strain was different from previously known strains, Sanger sequencing was performed directly from the patient's plasma. Biopsies obtained from autopsy were stained for immunohistochemistry.

RESULTS: The patient had approximately tenfold lower levels of PUUV neutralising antibodies and twice higher viral load than was normally seen for patients with less severe PUUV infection. We could demonstrate unique mutations in the S and M segments of the virus that could have had an impact on the severity of infection. Due to the severe course of infection, the patient was treated with the bradykinin receptor inhibitor icatibant to reduce bradykinin-mediated vessel permeability and maintain vascular circulation.

CONCLUSIONS: Our data suggest that bradykinin receptor inhibitor may not be highly efficient to treat patients that are at an advanced stage of HFRS. Low neutralising antibodies and high viral load at admission to the hospital were associated with the fatal outcome and may be useful for future predictions of disease outcome.

Emneord
Icatibant, Puumala orthohantavirus, neutralising antibodies, orthohantavirus, viral load, virus sequence
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-201272 (URN)10.1080/23744235.2022.2076904 (DOI)000812658600001 ()35713235 (PubMedID)2-s2.0-85132173959 (Scopus ID)
Forskningsfinansiär
Region Västerbotten, RV-938855Region Västerbotten, RV-734361Swedish Heart Lung Foundation, 2017-0334Swedish Research Council, 2020-06235Lars Hierta Memorial Foundation, FO2018- 0470
Tilgjengelig fra: 2022-11-25 Laget: 2022-11-25 Sist oppdatert: 2022-11-28bibliografisk kontrollert
Rosendal, E., Mihai, I. S., Becker, M., Das, D., Frängsmyr, L., Persson, B. D., . . . Lenman, A. (2022). Serine protease inhibitors restrict host susceptibility to SARS-CoV-2 infections. mBio, 13(3), Article ID e00892-22.
Åpne denne publikasjonen i ny fane eller vindu >>Serine protease inhibitors restrict host susceptibility to SARS-CoV-2 infections
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2022 (engelsk)Inngår i: mBio, ISSN 2161-2129, E-ISSN 2150-7511, Vol. 13, nr 3, artikkel-id e00892-22Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The coronavirus disease 2019, COVID-19, is a complex disease with a wide range of symptoms from asymptomatic infections to severe acute respiratory syndrome with lethal outcome. Individual factors such as age, sex, and comorbidities increase the risk for severe infections, but other aspects, such as genetic variations, are also likely to affect the susceptibility to SARS-CoV-2 infection and disease severity. Here, we used a human 3D lung cell model based on primary cells derived from multiple donors to identity host factors that regulate SARS-CoV-2 infection. With a transcriptomics-based approach, we found that less susceptible donors show a higher expression level of serine protease inhibitors SERPINA1, SERPINE1, and SERPINE2, identifying variation in cellular serpin levels as restricting host factors for SARS-CoV-2 infection. We pinpoint their antiviral mechanism of action to inhibition of the cellular serine protease, TMPRSS2, thereby preventing cleavage of the viral spike protein and TMPRSS2-mediated entry into the target cells. By means of single-cell RNA sequencing, we further locate the expression of the individual serpins to basal, ciliated, club, and goblet cells. Our results add to the importance of genetic variations as determinants for SARS-CoV-2 susceptibility and suggest that genetic deficiencies of cellular serpins might represent risk factors for severe COVID-19. Our study further highlights TMPRSS2 as a promising target for antiviral intervention and opens the door for the usage of locally administered serpins as a treatment against COVID-19.

sted, utgiver, år, opplag, sider
American Society for Microbiology, 2022
Emneord
A1AT, alpha-1-antitrypsin, antithrombin III, ATIII, COVID-19, PAI1, plasminogen activator inhibitor 1, SARS-CoV-2, serpin, TMPRSS2
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-203186 (URN)10.1128/mbio.00892-22 (DOI)000797888900001 ()35532162 (PubMedID)2-s2.0-85133144334 (Scopus ID)
Forskningsfinansiär
Science for Life Laboratory, SciLifeLabSwedish National Infrastructure for Computing (SNIC), SNIC 2020/6-251Swedish Heart Lung Foundation, 2020038Knut and Alice Wallenberg Foundation, 2020.0182Knut and Alice Wallenberg Foundation, C19R:028Swedish Society for Medical Research (SSMF)The Kempe Foundations, JCK-1827Swedish Research Council, 2016-06598
Tilgjengelig fra: 2023-01-17 Laget: 2023-01-17 Sist oppdatert: 2023-07-03bibliografisk kontrollert
Rankin, G. D., Kabéle, M., Brown, R., Macefield, V. G., Sandström, T. & Bosson, J. A. (2021). Acute Exposure to Diesel Exhaust Increases Muscle Sympathetic Nerve Activity in Humans. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 10(10), Article ID e018448.
Åpne denne publikasjonen i ny fane eller vindu >>Acute Exposure to Diesel Exhaust Increases Muscle Sympathetic Nerve Activity in Humans
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2021 (engelsk)Inngår i: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, E-ISSN 2047-9980, Vol. 10, nr 10, artikkel-id e018448Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Diesel exhaust (DE) emissions are a major contributor to ambient air pollution and are strongly associated with cardiovascular morbidity and mortality. Exposure to traffic-related particulate matter is linked with acute adverse cardiovascular events; however, the mechanisms are not fully understood. We examined the role of the autonomic nervous system during exposure to DE that has previously only been indirectly investigated.

Methods and Results: Using microneurography, we measured muscle sympathetic nerve activity (MSNA) directly in the peroneal nerve of 16 healthy individuals. MSNA, heart rate, and respiration were recorded while subjects rested breathing filtered air, filtered air with an exposure mask, and standardized diluted DE (300 µg/m3) through the exposure mask. Heart rate variability was assessed from an ECG. DE inhalation rapidly causes an increase in number of MSNA bursts as well as the size of bursts within 10 minutes, peaking by 30 minutes (P<0.001), compared with baseline filtered air with an exposure mask. No significant changes occurred in heart rate variability indices during DE exposure; however, MSNA frequency correlated negatively with total power (r2=0.294, P=0.03) and low frequency (r2=0.258, P=0.045). Heart rate correlated positively with MSNA frequency (r2=0.268, P=0.04) and the change in percentage of larger bursts (burst amplitude, height >50% of the maximum burst) from filtered air with an exposure mask (r2=0.368, P=0.013).

Conclusions: Our study provides direct evidence for the rapid modulation of the autonomic nervous system after exposure to DE, with an increase in MSNA. The quick increase in sympathetic outflow may explain the strong epidemiological data associating traffic-related particulate matter to acute adverse cardiovascular events such as myocardial infarction.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02892279.

sted, utgiver, år, opplag, sider
Wiley-Blackwell Publishing Inc., 2021
Emneord
air pollution, autonomic nervous system, diesel, heart rate variability, muscle sympathetic nerve activity, sympatho‐excitation
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-183918 (URN)10.1161/JAHA.120.018448 (DOI)000651436300025 ()33942621 (PubMedID)2-s2.0-85106552074 (Scopus ID)
Forskningsfinansiär
Swedish Heart Lung FoundationForte, Swedish Research Council for Health, Working Life and WelfareVästerbotten County Council
Tilgjengelig fra: 2021-06-04 Laget: 2021-06-04 Sist oppdatert: 2024-07-04bibliografisk kontrollert
Lepzien, R., Liu, S., Czarnewski, P., Nie, M., Österberg, B., Baharom, F., . . . Smed-Sörensen, A. (2021). Monocytes in sarcoidosis are potent tumour necrosis factor producers and predict disease outcome. European Respiratory Journal, 58(1), Article ID 2003468.
Åpne denne publikasjonen i ny fane eller vindu >>Monocytes in sarcoidosis are potent tumour necrosis factor producers and predict disease outcome
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2021 (engelsk)Inngår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 58, nr 1, artikkel-id 2003468Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Pulmonary sarcoidosis is an inflammatory disease characterised by granuloma formation and heterogeneous clinical outcome. Tumour necrosis factor (TNF) is a pro-inflammatory cytokine contributing to granuloma formation and high levels of TNF have been shown to associate with progressive disease. Mononuclear phagocytes (MNPs) are potent producers of TNF and highly responsive to inflammation. In sarcoidosis, alveolar macrophages have been well studied. However, MNPs also include monocytes/monocyte-derived cells and dendritic cells, which are poorly studied in sarcoidosis, despite their central role in inflammation.

Objective: To determine the role of pulmonary monocyte-derived cells and dendritic cells during sarcoidosis.

Methods: We performed in-depth phenotypic, functional and transcriptomic analysis of MNP subsets from blood and bronchoalveolar lavage (BAL) fluid from 108 sarcoidosis patients and 30 healthy controls. We followed the clinical development of patients and assessed how the repertoire and function of MNP subsets at diagnosis correlated with 2-year disease outcome.

Results: Monocytes/monocyte-derived cells were increased in blood and BAL of sarcoidosis patients compared to healthy controls. Interestingly, high frequencies of blood intermediate monocytes at time of diagnosis associated with chronic disease development. RNA sequencing analysis showed highly inflammatory MNPs in BAL of sarcoidosis patients. Furthermore, frequencies of BAL monocytes/monocyte-derived cells producing TNF without exogenous stimulation at time of diagnosis increased in patients that were followed longitudinally. In contrast to alveolar macrophages, the frequency of TNF-producing BAL monocytes/monocyte-derived cells at time of diagnosis was highest in sarcoidosis patients that developed progressive disease.

Conclusion: Our data show that pulmonary monocytes/monocyte-derived cells are highly inflammatory and can be used as a predictor of disease outcome in sarcoidosis patients.

sted, utgiver, år, opplag, sider
European Respiratory Society, 2021
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-186643 (URN)10.1183/13993003.03468-2020 (DOI)000697742000022 ()33446605 (PubMedID)2-s2.0-85111990276 (Scopus ID)
Tilgjengelig fra: 2021-08-20 Laget: 2021-08-20 Sist oppdatert: 2023-09-05bibliografisk kontrollert
Pourazar, J., Sehlstedt, M., Rankin, G., Uski, O., Boman, C., Lopez, N., . . . Muala, A. (2019). Exposure to wood smoke induced activation of lymphocyte subtypes in peripheral blood. Paper presented at European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.. European Respiratory Journal, 54
Åpne denne publikasjonen i ny fane eller vindu >>Exposure to wood smoke induced activation of lymphocyte subtypes in peripheral blood
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2019 (engelsk)Inngår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 54Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
sted, utgiver, år, opplag, sider
Sheffield: European Respiratory Society Journals, 2019
Emneord
Air pollution, Systemic effect, Inflammation
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-168164 (URN)10.1183/13993003.congress-2019.PA1983 (DOI)000507372402143 ()
Konferanse
European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.
Prosjekter
Bio4Energy
Forskningsfinansiär
Bio4Energy
Merknad

Supplement: 63. Meeting Abstract: PA1983.

Tilgjengelig fra: 2020-03-17 Laget: 2020-03-17 Sist oppdatert: 2024-07-02bibliografisk kontrollert
Lepzien, R., Rankin, G., Pourazar, J., Muala, A., Eklund, A., Grunewald, J., . . . Smed-Sorensen, A. (2019). Mapping mononuclear phagocytes in blood, lungs, and lymph nodes of sarcoidosis patients. Journal of Leukocyte Biology, 105(4), 797-807
Åpne denne publikasjonen i ny fane eller vindu >>Mapping mononuclear phagocytes in blood, lungs, and lymph nodes of sarcoidosis patients
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2019 (engelsk)Inngår i: Journal of Leukocyte Biology, ISSN 0741-5400, E-ISSN 1938-3673, Vol. 105, nr 4, s. 797-807Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Sarcoidosis is a T-cell driven inflammatory disease characterized by granuloma formation. Mononuclear phagocytes (MNPs)-macrophages, monocytes, and dendritic cells (DCs)-are likely critical in sarcoidosis as they initiate and maintain T cell activation and contribute to granuloma formation by cytokine production. Granulomas manifest primarily in lungs and lung-draining lymph nodes (LLNs) but these compartments are less studied compared to blood and bronchoalveolar lavage (BAL). Sarcoidosis can present with an acute onset (usually Lofgren's syndrome (LS)) or a gradual onset (non-LS). LS patients typically recover within 2 years while 60% of non-LS patients maintain granulomas for up to 5 years. Here, four LS and seven non-LS patients underwent bronchoscopy with endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). From each patient, blood, BAL, endobronchial biopsies (EBBs), and LLN samples obtained by EBUS-TBNA were collected and MNPs characterized using multicolor flow cytometry. Six MNP subsets were identified at varying frequencies in the anatomical compartments investigated. Importantly, monocytes and DCs were most mature with migratory potential in BAL and EBBs but not in the LLNs suggesting heterogeneity in MNPs in the compartments typically affected in sarcoidosis. Additionally, in LS patients, frequencies of DC subsets were lower or lacking in LLNs and EBBs, respectively, compared to non-LS patients that may be related to the disease outcome. Our work provides a foundation for future investigations of MNPs in sarcoidosis to identify immune profiles of patients at risk of developing severe disease with the aim to provide early treatment to slow down disease progression.

sted, utgiver, år, opplag, sider
Society for Leukocyte Biology, 2019
Emneord
dendritic cell, monocyte, sarcoidosis, lymph node, Lofgren's syndrome
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-158084 (URN)10.1002/JLB.5A0718-280RR (DOI)000462155000015 ()30742337 (PubMedID)2-s2.0-85061445996 (Scopus ID)
Forskningsfinansiär
Swedish Heart Lung FoundationSwedish Research Council
Tilgjengelig fra: 2019-04-15 Laget: 2019-04-15 Sist oppdatert: 2023-05-09bibliografisk kontrollert
Rankin, G., Byström, J. W., Gustafsson, R., Hansson, M., Thunberg, T., Ahlm, C. & Connolly, A.-M. F. (2019). MMP9 Associates with Endothelial Glycocalyx Degradation During Haemorrhagic Fever with Renal Syndrome. Paper presented at 3rd Joint Meeting of the European-Society-for-Microcirculation (ESM) and the European-Vascular-Biology-Organization (EVBO), Maastricht, Netherlands, April, 2019.. Journal of Vascular Research, 56, 35-35
Åpne denne publikasjonen i ny fane eller vindu >>MMP9 Associates with Endothelial Glycocalyx Degradation During Haemorrhagic Fever with Renal Syndrome
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2019 (engelsk)Inngår i: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 56, s. 35-35Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
Abstract [en]

Introduction: Haemorrhagic fever with renal syndrome (HFRS) is characterized by fever, hypotension, vascular leakage, thrombocytopenia and renal failure. HFRS in Sweden is caused by the Puumala hantavirus and is spread by viral-infested droppings from bank voles. The health care system has little to offer these patients since there is no antiviral treatment and as of yet there is no vaccine prophylaxis available. We previously showed that a marker of endothelial glycocalyx degradation (Syndecan-1) was associated with disease severity and disseminated intravascular coagulation during HFRS (Connolly-Andersen et al., 2014, Open Forum Infect Dis.).

Methods: We analysed the levels of other endothelial glycocalyx degradation markers (heparan sulfate, soluble thrombomodulin, albumin), a potential “sheddase”: Matrix Metalloproinase 9 (MMP9) and neutrophil activation/tissue damage (neutrophil gelatinase-associated lipocalin, NGAL) in patient plasma from 44 HFRS patients collected consecutively following disease onset. We used the generalized estimating equation to analyse the association between endothelial glycocalyx degradation, MMP9 levels, neutrophil activation/tissue damage and HFRS disease outcome (need for oxygen, transfusion with blood components, need for intensive care unit (ICU) treatment and renal damage).

Results: 44 HFRS patients were included in this study (29 females (66%)); need for oxygen: 11 (25%); transfusion with blood components: 3 (7%) and stay at ICU: 2 (5%)). The levels of MMP9 were significantly associated with all markers of endothelial glycocalyx degradation. Neutrophil activation/tissue damage (NGAL) was also significantly associated with MMP9 and endothelial glycocalyx degradation markers (apart from albumin (p = 0.053). In addition degradation of endothelial glycocalyx associated with HFRS disease outcome.

Conclusion: Degradation of the endothelial glycocalyx could be a potential mechanism of HFRS pathogenesis, and potentially MMP9 could contribute to degradation of the endothelial glycocalyx

sted, utgiver, år, opplag, sider
S. Karger, 2019
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-158767 (URN)10.1159/000499516 (DOI)000463529300074 ()
Konferanse
3rd Joint Meeting of the European-Society-for-Microcirculation (ESM) and the European-Vascular-Biology-Organization (EVBO), Maastricht, Netherlands, April, 2019.
Merknad

Supplement 1, meeting abstract 73.

Tilgjengelig fra: 2019-05-08 Laget: 2019-05-08 Sist oppdatert: 2020-07-30bibliografisk kontrollert
Organisasjoner
Identifikatorer
ORCID-id: ORCID iD iconorcid.org/0000-0002-8753-830x