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Särndahl, Eva
Publications (10 of 35) Show all publications
Hylén, U., Eklund, D., Humble, M. B., Bartoszek, J., Särndahl, E. & Bejerot, S. (2020). Increased inflammasome activity in markedly ill psychiatric patients: An explorative study. Journal of Neuroimmunology, 339, Article ID 577119.
Open this publication in new window or tab >>Increased inflammasome activity in markedly ill psychiatric patients: An explorative study
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2020 (English)In: Journal of Neuroimmunology, ISSN 0165-5728, E-ISSN 1872-8421, Vol. 339, article id 577119Article in journal (Refereed) Published
Abstract [en]

The aim of this study was to investigate inflammatory perturbations in 40 patients with severe and complex psychiatric disorders by studying the activity of the NLRP3 inflammasome, with a trans-diagnostic approach. Gene expression of CASP1, NLRP3, PYCARD, IL1B, IL1RN, TNF showed a significant increase in the patient group compared to a matched control group. Plasma levels of IL1Ra, IL-18, TNF, IL-6 and CRP were increased in the patient group. Within the patient group, increased gene expression of inflammatory markers correlated with increased disease severity. The findings support the inflammation hypothesis for markedly ill psychiatric patients across diagnostic groups.

Place, publisher, year, edition, pages
Elsevier, 2020
National Category
Psychiatry Immunology in the medical area
Identifiers
urn:nbn:se:oru:diva-79288 (URN)10.1016/j.jneuroim.2019.577119 (DOI)000510528000013 ()31786499 (PubMedID)2-s2.0-85075532475 (Scopus ID)
Note

Funding Agencies:

Region Örebro County (ALF)  

Region Örebro County (Research Committee)  

Faculty of Medicine and Health, Örebro University 

Available from: 2020-01-21 Created: 2020-01-21 Last updated: 2020-03-17Bibliographically approved
Hedbrant, A., Andersson, L., Bryngelsson, I.-L., Eklund, D., Westberg, H., Särndahl, E. & Persson, A. (2020). Quartz Dust Exposure Affects NLRP3 Inflammasome Activation and Plasma Levels of IL-18 and IL-1Ra in Iron Foundry Workers. Mediators of Inflammation, Article ID 8490908.
Open this publication in new window or tab >>Quartz Dust Exposure Affects NLRP3 Inflammasome Activation and Plasma Levels of IL-18 and IL-1Ra in Iron Foundry Workers
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2020 (English)In: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, article id 8490908Article in journal (Refereed) Published
Abstract [en]

Purpose: To study the association between inhalation of particulate matter or quartz in Swedish iron foundries and the effects on NLRP3 inflammasome activation. 

Methods: Particle exposure measurements were performed during an eight-hour work day for 85 foundry workers at three Swedish iron foundries. Personal sampling was used for measurement of respirable quartz and dust and stationary measurements to obtain exposure measurements for inhalable dust and PM10. The NLRP3 inflammasome markers, interleukin- (IL-) 1β and IL-18, and inhibitors IL-1 receptor antagonist (IL-1Ra) and IL-18 binding protein (IL-18BP) were measured in plasma. Inflammasome activation was measured by caspase-1 enzymatic activity in monocytes in whole blood by flow cytometry, and expression of inflammasome-related genes was quantified using real-time PCR. Multiple linear regression analysis was used to investigate associations between PM exposures and inflammatory markers. Sex, age, smoking, current infection, BMI, and single nucleotide polymorphism in the inflammasome regulating genes CARD8 (C10X) and NLRP3 (Q705K) were included as covariates. 

Results: The average exposure levels of respirable dust and quartz were 0.85 and 0.052 mg/m3, respectively. A significant exposure-response was found for respirable dust and IL-18 and for inhalable dust and IL-1Ra. Whole blood, drawn from study participants, was stimulated ex vivo with inflammasome priming stimuli LPS or Pam3CSK4, resulting in a 47% and 49% increase in caspase-1 enzymatic activity in monocytes. This increase in caspase-1 activity was significantly attenuated in the higher exposure groups for most PM exposure measures. 

Conclusions: The results indicate that exposure levels of PM in the iron foundry environment can affect the NLRP3 inflammasome and systemic inflammation.

Place, publisher, year, edition, pages
Hindawi Publishing Corporation, 2020
National Category
Occupational Health and Environmental Health
Research subject
Occupational and Environmental Medicine; Immunology
Identifiers
urn:nbn:se:oru:diva-79441 (URN)10.1155/2020/8490908 (DOI)000508370800002 ()2-s2.0-85078206275 (Scopus ID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2014-0802Knowledge Foundation, 20150036
Note

Funding Agency:

Örebro University  ORU 2.2.1-4060/2013

Available from: 2020-01-28 Created: 2020-01-28 Last updated: 2020-03-17Bibliographically approved
Rasmussen, G., Asfaw Idosa, B., Monecke, S., Bäckman, A., Strålin, K., Särndahl, E. & Söderquist, B. (2019). Caspase-1 Inflammasome Activity in Patients with Staphylococcus aureus Bacteremia. Microbiology and immunology, 63(12), 487-499
Open this publication in new window or tab >>Caspase-1 Inflammasome Activity in Patients with Staphylococcus aureus Bacteremia
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2019 (English)In: Microbiology and immunology, ISSN 0385-5600, E-ISSN 1348-0421, Vol. 63, no 12, p. 487-499Article in journal (Refereed) Published
Abstract [en]

The inflammasome is a multiprotein complex that mediates caspase-1 activation with subsequent maturation of the pro-inflammatory cytokines IL-1β and IL-18. The NLRP3 inflammasome is known to be activated by Staphylococcus aureus, one of the leading causes of bacteremia worldwide. Inflammasome activation and regulation in response to bacterial infection have been found to be of importance for a balanced host immune response. However, inflammasome signaling in vivo in humans initiated by S. aureus is currently sparsely studied. The present study therefore aimed to investigate NLRP3 inflammasome activity in 20 S. aureus bacteremia patients, by repeated measurement during the first week of bacteremia, compared with controls. Caspase-1 activity was measured in monocytes and neutrophils by flow cytometry detecting FLICA (Fluorescent Labelled Inhibitor of Caspase-1), while IL-1β and IL-18 was measured by Luminex and ELISA, respectively. As a measure of inflammasome priming, mRNA expression of NLRP3, CASP1 (pro-caspase-1) and IL1B (pro-IL-1β) was analyzed by qPCR. We found induced caspase-1 activity in innate immune cells with subsequent release of IL-18 in patients during the acute phase of bacteremia, indicating activation of the inflammasome. There was substantial inter-individual variation in caspase-1 activity between S. aureus bacteremia patients. We also found an altered inflammasome priming with low mRNA levels of NLRP3 accompanied by elevated mRNA levels of IL1B. This increased knowledge of the individual host immune response in S. aureus bacteremia could provide support in the effort to optimize management and treatment of each individual patient.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2019
Keywords
Caspase-1, NLRP3, Staphylococcus aureus, sepsis
National Category
Immunology
Identifiers
urn:nbn:se:oru:diva-75829 (URN)10.1111/1348-0421.12738 (DOI)000490350100001 ()31403210 (PubMedID)
Note

Funding Agencies:

Nyckelfonden in Region Örebro County, Sweden  

Region Örebro County's Research Committee, Sweden  

ALF research funding in Region Örebro County, Sweden  

Available from: 2019-08-23 Created: 2019-08-23 Last updated: 2019-12-19Bibliographically approved
Westberg, H., Hedbrant, A., Persson, A., Bryngelsson, I.-L., Johansson, A., Ericsson, A., . . . Andersson, L. (2019). Inflammatory and coagulatory markers and exposure to different size fractions of particle mass, number and surface area air concentrations in Swedish iron foundries, in particular respirable quartz. International Archives of Occupational and Environmental Health, 92(8), 1087-1098
Open this publication in new window or tab >>Inflammatory and coagulatory markers and exposure to different size fractions of particle mass, number and surface area air concentrations in Swedish iron foundries, in particular respirable quartz
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2019 (English)In: International Archives of Occupational and Environmental Health, ISSN 0340-0131, E-ISSN 1432-1246, Vol. 92, no 8, p. 1087-1098Article in journal (Refereed) Published
Abstract [en]

PURPOSE: To study the relationship between inhalation of airborne particles and quartz in Swedish iron foundries and markers of inflammation and coagulation in blood.

METHODS: Personal sampling of respirable dust and quartz was performed for 85 subjects in three Swedish iron foundries. Stationary measurements were used to study the concentrations of respirable dust and quartz, inhalable and total dust, PM10 and PM2.5, as well as the particle surface area and the particle number concentrations. Markers of inflammation, namely interleukins (IL-1β, IL-6, IL-8, IL-10 and IL-12), C-reactive protein, and serum amyloid A (SAA) were measured in plasma or serum, together with markers of coagulation including fibrinogen, factor VIII (FVIII), von Willebrand factor and D-dimer. Complete sampling was performed on the second or third day of a working week after a work-free weekend, and follow-up samples were collected 2 days later. A mixed model analysis was performed including sex, age, smoking, infections, blood group, sampling day and BMI as covariates.

RESULTS: The average 8-h time-weighted average air concentrations of respirable dust and quartz were 0.85 mg/m3 and 0.052 mg/m3, respectively. Participants in high-exposure groups with respect to some of the measured particle types exhibited significantly elevated levels of SAA, fibrinogen and FVIII.

CONCLUSIONS: These observed relationships between particle exposure and inflammatory markers may indicate an increased risk of cardiovascular disease among foundry workers with high particulate exposure.

Place, publisher, year, edition, pages
Springer Berlin/Heidelberg, 2019
Keywords
Inflammatory markers, Iron foundries, Particle mass, Particle number, Particle surface area, Respirable quartz
National Category
Occupational Health and Environmental Health
Research subject
Occupational and Environmental Medicine; Biomedicine
Identifiers
urn:nbn:se:oru:diva-76003 (URN)10.1007/s00420-019-01446-z (DOI)000492593000002 ()31165309 (PubMedID)2-s2.0-85067255425 (Scopus ID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2014-0802Knowledge Foundation, 20150036
Note

Funding Agency:

Örebro University  ORU 2.2.1-4060/2013

Available from: 2019-09-02 Created: 2019-09-02 Last updated: 2019-11-15Bibliographically approved
Asfaw Idosa, B., Kelly, A., Jacobsson, S., Demirel, I., Fredlund, H., Särndahl, E. & Persson, A. (2019). Neisseria meningitidis-Induced Caspase-1 Activation in Human Innate Immune Cells Is LOS-Dependent. Journal of Immunology Research, Article ID 6193186.
Open this publication in new window or tab >>Neisseria meningitidis-Induced Caspase-1 Activation in Human Innate Immune Cells Is LOS-Dependent
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2019 (English)In: Journal of Immunology Research, ISSN 2314-8861, E-ISSN 2314-7156, article id 6193186Article in journal (Refereed) Published
Abstract [en]

Meningococcal disease such as sepsis and meningitidis is hallmarked by an excessive inflammatory response. The causative agent, Neisseria meningitidis, expresses the endotoxin lipooligosaccharide (LOS) that is responsible for activation of immune cells and the release of proinflammatory cytokines. One of the most potent proinflammatory cytokines, interleukin-1 (IL-1), is activated following caspase-1 activity in the intracellular multiprotein complex called inflammasome. Inflammasomes are activated by a number of microbial factors as well as danger molecules by a two-step mechanismpriming and licensing of inflammasome activationbut there are no data available regarding a role for inflammasome activation in meningococcal disease. The aim of this study was to investigate if N. meningitidis activates the inflammasome and, if so, the role of bacterial LOS in this activation. Cells were subjected to N. meningitidis, both wild-type (FAM20) and its LOS-deficient mutant (lpxA), and priming as well as licensing of inflammasome activation was investigated. The wild-type LOS-expressing parental FAM20 serogroup C N. meningitidis (FAM20) strain significantly enhanced the caspase-1 activity in human neutrophils and monocytes, whereas lpxA was unable to induce caspase-1 activity as well as to induce IL-1 release. While the lpxA mutant induced a priming response, measured as increased expression of NLRP3 and IL1B, the LOS-expressing FAM20 further increased this priming. We conclude that although non-LOS components of N. meningitidis contribute to the priming of the inflammasome activity, LOS per se is to be considered as the central component of N. meningitidis virulence, responsible for both priming and licensing of inflammasome activation.

Place, publisher, year, edition, pages
Hindawi Publishing Corporation, 2019
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:oru:diva-74647 (URN)10.1155/2019/6193186 (DOI)000468500900001 ()
Available from: 2019-06-10 Created: 2019-06-10 Last updated: 2019-06-10Bibliographically approved
Andersson, L., Bryngelsson, I.-L., Hedbrant, A., Persson, A., Johansson, A., Ericsson, A., . . . Westberg, H. (2019). Respiratory health and inflammatory markers: Exposure to respirable dust and quartz and chemical binders in Swedish iron foundries. PLoS ONE, 14(11), Article ID e0224668.
Open this publication in new window or tab >>Respiratory health and inflammatory markers: Exposure to respirable dust and quartz and chemical binders in Swedish iron foundries
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2019 (English)In: PLoS ONE, E-ISSN 1932-6203, Vol. 14, no 11, article id e0224668Article in journal (Refereed) Published
Abstract [en]

PURPOSE: To study the relationship between respirable dust, quartz and chemical binders in Swedish iron foundries and respiratory symptoms, lung function (as forced expiratory volume FEV1 and vital capacity FVC), fraction of exhaled nitric oxide (FENO) and levels of club cell secretory protein 16 (CC16) and CRP.

METHODS: Personal sampling of respirable dust and quartz was performed for 85 subjects in three Swedish iron foundries. Full shift sampling and examination were performed on the second or third day of a working week after a work free weekend, with additional sampling on the fourth or fifth day. Logistic, linear and mixed model analyses were performed including, gender, age, smoking, infections, sampling day, body mass index (BMI) and chemical binders as covariates.

RESULTS: The adjusted average respirable quartz and dust concentrations were 0.038 and 0.66 mg/m3, respectively. Statistically significant increases in levels of CC16 were associated with exposure to chemical binders (p = 0.05; p = 0.01) in the regression analysis of quartz and respirable dust, respectively. Non-significant exposure-responses were identified for cumulative quartz and the symptoms asthma and breathlessness. For cumulative chemical years, non-significant exposure-response were observed for all but two symptoms. FENO also exhibited a non significant exposure-response for both quartz and respirable dust. No exposure-response was determined for FEV1 or FVC, CRP and respirable dust and quartz.

CONCLUSIONS: Our findings suggest that early markers of pulmonary effect, such as increased levels of CC16 and FENO, are more strongly associated with chemical binder exposure than respirable quartz and dust in foundry environments.

Place, publisher, year, edition, pages
PLOS, 2019
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:oru:diva-77712 (URN)10.1371/journal.pone.0224668 (DOI)000532673600017 ()31675355 (PubMedID)2-s2.0-85074400397 (Scopus ID)
Funder
Forte, Swedish Research Council for Health, Working Life and Welfare, 2014-0802Knowledge Foundation, 20150036
Note

Funding Agency:

Örebro University  ORU 2.2.1-4060/2013

Available from: 2019-11-07 Created: 2019-11-07 Last updated: 2020-05-29Bibliographically approved
Demirel, I., Persson, A., Brauner, A., Särndahl, E., Kruse, R. & Persson, K. (2018). Activation of the NLRP3 Inflammasome Pathway by Uropathogenic Escherichia coli Is Virulence Factor-Dependent and Influences Colonization of Bladder Epithelial Cells. Frontiers in Cellular and Infection Microbiology, 8, Article ID 81.
Open this publication in new window or tab >>Activation of the NLRP3 Inflammasome Pathway by Uropathogenic Escherichia coli Is Virulence Factor-Dependent and Influences Colonization of Bladder Epithelial Cells
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2018 (English)In: Frontiers in Cellular and Infection Microbiology, E-ISSN 2235-2988, Vol. 8, article id 81Article in journal (Refereed) Published
Abstract [en]

The NLRP3 inflammasome and IL-1 beta release have recently been suggested to be important for the progression of urinary tract infection (UTI). However, much is still unknown regarding the interaction of UPEC and the NLRP3 inflammasome. The purpose of this study was to elucidate what virulence factors uropathogenic Escherichia coil (UPEC) use to modulate NLRP3 inflammasome activation and subsequent IL-1 beta release and the role of NLRP3 for UPEC colonization of bladder epithelial cells. The bladder epithelial cell line 5637, CRISPR/Cas9 generated NLRP3, caspase-1 and mesotrypsin deficient cell lines and transformed primary bladder epithelial cells (HBLAK) were stimulated with UPEC isolates and the non-pathogenic MG1655 strain. We found that the UPEC strain CFT073, but not MG1655, induced an increased caspase-1 activity and IL-1 beta release from bladder epithelial cells. The increase was shown to be mediated by et-hemolysin activation of the NLRP3 inflammasome in an NE-kappa B-independent manner. The effect of-hemolysin on IL-1 beta release was biphasic, initially suppressive, later inductive. Furthermore, the phase-locked type-1-fimbrial ON variant of CFT073 inhibited caspase-1 activation and IL-1 beta release. In addition, the ability of CFT073 to adhere to and invade NLRP3 deficient cells was significantly reduced compare to wild-type cells. The reduced colonization of NLRP3-deficient cells was type-1 fimbriae dependent. In conclusion, we found that the NLRP3 inflammasome was important for type-1 fimbriae-dependent colonization of bladder epithelial cells and that both type-1 fimbriae and alpha-hemolysin can modulate the activity of the NLRP3 inflammasome.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2018
Keywords
UPEC, NLRP3 inflammasome, IL-1 beta, alpha-hemolysin, type-1 fimbriae
National Category
Immunology in the medical area Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-66388 (URN)10.3389/fcimb.2018.00081 (DOI)000427407100001 ()2-s2.0-85043771169 (Scopus ID)
Note

Funding Agency:

Faculty of Medicine and Health at Örebro University 

Available from: 2018-04-09 Created: 2018-04-09 Last updated: 2018-08-20Bibliographically approved
Månsson, E., Sahdo, B., Nilsdotter-Augustinsson, Å., Särndahl, E. & Söderquist, B. (2018). Lower activation of caspase-1 by Staphylococcus epidermidis isolated from prosthetic joint infections compared to commensals. Journal of bone and joint infection, 3(1), 10-14
Open this publication in new window or tab >>Lower activation of caspase-1 by Staphylococcus epidermidis isolated from prosthetic joint infections compared to commensals
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2018 (English)In: Journal of bone and joint infection, ISSN 2206-3552, Vol. 3, no 1, p. 10-14Article in journal (Refereed) Published
Abstract [en]

Nosocomial sequence types of Staphylococcus epidermidis dominate in prosthetic joint infections. We examined caspase-1 activation in human neutrophils after incubation with Staphylococcus epidermidis isolated from prosthetic joint infections and normal skin flora. Active caspase-1 was lower after incubation with isolates from prosthetic joint infections than after incubation with commensal isolates. Both host and isolate dependent differences in active caspase-1 were noted. Our results indicate that there might be a host-dependent incapacity to elicit a strong caspase-1 response towards certain strains of S. epidermidis. Further experiments with a larger number of individuals are warranted.

Place, publisher, year, edition, pages
IVYSPRING, 2018
Keywords
Staphylococcus epidermidis, caspase-1, neutrophils, prosthetic joint infections, host-pathogen interaction
National Category
Medical and Health Sciences Infectious Medicine
Identifiers
urn:nbn:se:oru:diva-65927 (URN)10.7150/jbji.21567 (DOI)29545990 (PubMedID)
Available from: 2018-03-21 Created: 2018-03-21 Last updated: 2018-09-04Bibliographically approved
Månsson, E., Söderquist, B., Nilsdotter-Augustinsson, Å., Särndahl, E. & Demirel, I. (2018). Staphylococcus epidermidis from prosthetic joint infections induces lower IL-1 release from human neutrophils than isolates from normal flora. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 126(8), 678-684
Open this publication in new window or tab >>Staphylococcus epidermidis from prosthetic joint infections induces lower IL-1 release from human neutrophils than isolates from normal flora
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2018 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 126, no 8, p. 678-684Article in journal (Refereed) Published
Abstract [en]

The aim of this study was to test the hypothesis that Staphylococcus epidermidis isolated from prosthetic joint infections (PJIs) differs from S.epidermidis isolated from normal flora in terms of its capacity to induce activation of caspase-1 and release of IL-1 in human neutrophils. The amount of active caspase-1 was determined over 6h by detecting Ac-YVAD-AMC fluorescence in human neutrophils incubated with S.epidermidis isolates from PJIs (ST2) or normal flora. The amount of IL-1 was detected by ELISA in neutrophil supernatants after 6h of incubation. Mean IL-1 release was lower after incubation with S.epidermidis from PJIs compared to isolates from normal flora, but no statistically significant difference was found in active caspase-1. Substantial inter-individual differences in both active caspase-1 and IL-1 were noted. These results suggest that evasion of innate immune response, measured as reduced capacity to induce release of IL-1 from human neutrophils, might be involved in the predominance of ST2 in S.epidermidis PJIs, but that other microbe-related factors are probably also important.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2018
Keywords
Staphylococcus epidermidis, prosthesis-related infections, pathology, host-pathogen interactions, immunology, caspase-1, interleukin-1beta
National Category
Immunology in the medical area Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-68468 (URN)10.1111/apm.12861 (DOI)000440136000004 ()2-s2.0-85050768159 (Scopus ID)
Available from: 2018-08-15 Created: 2018-08-15 Last updated: 2018-09-07Bibliographically approved
Bergström, I., Lundberg, A. K., Jönsson, S., Särndahl, E., Ernerudh, J. & Jonasson, L. (2017). Annexin A1 in blood mononuclear cells from patients with coronary artery disease: Its association with inflammatory status and glucocorticoid sensitivity. PLoS ONE, 12(3), Article ID e0174177.
Open this publication in new window or tab >>Annexin A1 in blood mononuclear cells from patients with coronary artery disease: Its association with inflammatory status and glucocorticoid sensitivity
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2017 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 3, article id e0174177Article in journal (Refereed) Published
Abstract [en]

Annexin A1 (AnxA1) is a key player in resolution of inflammation and a mediator of glucocorticoid actions. In atherosclerotic tissue, increased expression of AnxA1 has been associated with protective plaque-stabilizing effects. Here, we investigated the expression of AnxA1 in peripheral blood mononuclear cells (PBMCs) from patients with coronary artery disease (CAD). Blood was collected from 57 patients with stable CAD (SCAD) and 41 healthy controls. We also included a minor group (n = 10) with acute coronary syndrome (ACS). AnxA1 mRNA was measured in PBMCs. Expression of AnxA1 protein (total and surface-bound) and glucocorticoid receptors (GR) were detected in PBMC subsets by flow cytometry. Also, salivary cortisol, interleukin(IL)-6 and IL-10 in plasma, and LPS-induced cytokine secretion from PBMCs, with or without dexamethasone, were assessed. AnxA1 mRNA was found to be slightly increased in PBMCs from SCAD patients compared with controls. However, protein expression of AnxA1 or GRs in PBMC subsets did not differ between SCAD patients and controls, despite SCAD patients showing a more proinflammatory cytokine profile ex vivo. Only surface expression of AnxA1 on monocytes correlated with dexamethasone-mediated suppression of cytokines. In ACS patients, a marked activation of AnxA1 was seen involving both gene expression and translocation of protein to cell surface probably reflecting a rapid glucocorticoid action modulating the acute inflammatory response in ACS. To conclude, surface expression of AnxA1 on monocytes may reflect the degree of glucocorticoid sensitivity. Speculatively, "normal" surface expression of AnxA1 indicates that anti-inflammatory capacity is impaired in SCAD patients.

Place, publisher, year, edition, pages
Public Library of Science, 2017
National Category
General Practice Immunology in the medical area
Identifiers
urn:nbn:se:oru:diva-57677 (URN)10.1371/journal.pone.0174177 (DOI)000399094700065 ()28329022 (PubMedID)2-s2.0-85016084129 (Scopus ID)
Funder
Swedish Research Council, K2015-65x-14599-13-3Swedish Heart Lung Foundation, 20150648
Available from: 2017-05-16 Created: 2017-05-16 Last updated: 2018-01-13Bibliographically approved
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