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Andersson, Henrik
Publications (9 of 9) Show all publications
Snygg, J., Andersson, H., Fredrikson, M. & Chew, M. S. (2019). Myocardial injury in noncardiac surgery in Sweden: Study protocol for a multicentre, observational cohort study of patients undergoing elective, major abdominal surgery. European Journal of Anaesthesiology, 36(5), 383-385
Open this publication in new window or tab >>Myocardial injury in noncardiac surgery in Sweden: Study protocol for a multicentre, observational cohort study of patients undergoing elective, major abdominal surgery
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2019 (English)In: European Journal of Anaesthesiology, ISSN 0265-0215, E-ISSN 1365-2346, Vol. 36, no 5, p. 383-385Article in journal (Other academic) Published
Abstract [en]

[No abstract available]

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2019
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:liu:diva-160142 (URN)10.1097/EJA.0000000000000976 (DOI)000480686500015 ()30946177 (PubMedID)2-s2.0-85064239257 (Scopus ID)
Available from: 2019-09-09 Created: 2019-09-09 Last updated: 2019-09-19Bibliographically approved
Shabo, I., Midtbö, K. M., Andersson, H., Åkerlund, E., Olsson, H., Wegman, P., . . . Lindström, A. (2015). Macrophage traits in cancer cells are induced by macrophage-cancer cell fusion and cannot be explained by cellular interaction. BMC Cancer, 15(1), 922
Open this publication in new window or tab >>Macrophage traits in cancer cells are induced by macrophage-cancer cell fusion and cannot be explained by cellular interaction
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2015 (English)In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 15, no 1, p. 922-Article in journal (Refereed) Published
Abstract [en]

Background: Cell fusion is a natural process in normal development and tissue regeneration. Fusion between cancer cells and macrophages generates metastatic hybrids with genetic and phenotypic characteristics from both maternal cells. However, there are no clinical markers for detecting cell fusion in clinical context. Macrophage-specific antigen CD163 expression in tumor cells is reported in breast and colorectal cancers and proposed being caused by macrophages-cancer cell fusion in tumor stroma. The purpose of this study is to examine the cell fusion process as a biological explanation for macrophage phenotype in breast. Methods: Monocytes, harvested from male blood donor, were activated to M2 macrophages and co-cultured in ThinCert transwell system with GFP-labeled MCF-7 cancer cells. MCF7/macrophage hybrids were generated by spontaneous cell fusion, isolated by fluorescence-activated cell sorting and confirmed by fluorescence microscopy, short tandem repeats analysis and flow cytometry. CD163 expression was evaluated in breast tumor samples material from 127 women by immunohistochemistry. Results: MCF-7/macrophage hybrids were generated spontaneously at average rate of 2 % and showed phenotypic and genetic traits from both maternal cells. CD163 expression in MCF-7 cells could not be induced by paracrine interaction with M2-activated macrophages. CD163 positive cancer cells in tumor sections grew in clonal collection and a cutoff point greater than25 % of positive cancer cells was significantly correlated to disease free and overall survival. Conclusions: In conclusion, macrophage traits in breast cancer might be caused by cell fusion rather than explained by paracrine cellular interaction. These data provide new insights into the role of cell fusion in breast cancer and contributes to the development of clinical markers to identify cell fusion.

Place, publisher, year, edition, pages
BIOMED CENTRAL LTD, 2015
Keywords
Cell fusion; Macrophages; Paracrine cellular interaction; Tumor markers
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-123328 (URN)10.1186/s12885-015-1935-0 (DOI)000365276000001 ()26585897 (PubMedID)
Note

Funding Agencies|County Council of Ostergotland (Sweden); National Organization of Breast Cancer Associations (Sweden); Bengt Ihre Foundation (Swedish Surgical Society)

Available from: 2015-12-14 Created: 2015-12-11 Last updated: 2018-01-10
Andersson, H., Björnström-Karlsson, K., Eintrei, C. & Sundqvist, T. (2015). Orexin A Phosphorylates the gamma-Aminobutyric Acid Type A Receptor beta(2) Subunit on a Serine Residue and Changes the Surface Expression of the Receptor in SH-SY5Y Cells Exposed to Propofol. Journal of Neuroscience Research, 93(11), 1748-1755
Open this publication in new window or tab >>Orexin A Phosphorylates the gamma-Aminobutyric Acid Type A Receptor beta(2) Subunit on a Serine Residue and Changes the Surface Expression of the Receptor in SH-SY5Y Cells Exposed to Propofol
2015 (English)In: Journal of Neuroscience Research, ISSN 0360-4012, E-ISSN 1097-4547, Vol. 93, no 11, p. 1748-1755Article in journal (Refereed) Published
Abstract [en]

Propofol activates the gamma-aminobutyric acid type A receptor (GABA(A)R) and causes a reversible neurite retraction, leaving a thin, thread-like structure behind; it also reverses the transport of vesicles in rat cortical neurons. The awakening peptide orexin A (OA) inhibits this retraction via phospholipase D (PLD) and protein kinase CE (PKCE). The human SH-SY5Y cells express both GABA(A)Rs and orexin 1 and 2 receptors. These cells are used to examine the interaction between OA and the GABAAR. The effects of OA are studied with flow cytometry and immunoblotting. This study shows that OA stimulates phosphorylation on the serine residues of the GABA(A)R beta(2) subunit and that the phosphorylation is caused by the activation of PLD and PKCE. OA administration followed by propofol reduces the cell surface expression of the GABA(A)R, whereas propofol stimulation before OA increases the surface expression. The GABA(A)R beta(2) subunit is important for receptor recirculation, and the effect of OA on propofol-stimulated cells may be due to a disturbed recirculation of the GABA(A)R. (C) 2015 Wiley Periodicals, Inc.

Place, publisher, year, edition, pages
WILEY-BLACKWELL, 2015
Keywords
orexin; propofol; GABAAR; cell signaling; AB_10675844; AB_1269637; AB_10712311; AB_2247467; AB_307187; AB_307184; AB_1566589
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-122517 (URN)10.1002/jnr.23631 (DOI)000362831800013 ()26283475 (PubMedID)
Note

Funding Agencies|County Council of Ostergotland ALF Grants; Linkoping University Hospital; Ella and Henry Stahl Research Foundation

Available from: 2015-11-09 Created: 2015-11-06 Last updated: 2018-01-10
Abuzeid, N., Kalsum, S., Koshy, R. J., Larsson, M. C., Glader, M., Andersson, H., . . . Lerm, M. (2014). Antimycobacterial activity of selected medicinal plants traditionally used in Sudan to treat infectious diseases. Journal of Ethnopharmacology, 157, 134-139
Open this publication in new window or tab >>Antimycobacterial activity of selected medicinal plants traditionally used in Sudan to treat infectious diseases
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2014 (English)In: Journal of Ethnopharmacology, ISSN 0378-8741, E-ISSN 1872-7573, Vol. 157, p. 134-139Article in journal (Refereed) Published
Abstract [en]

Ethnopharmacological relevance: The emergence of multidrug-resistant strains of Mycobacterium tuberculosis underscores the need for continuous development of new and efficient methods to determine the susceptibility of isolates of Mycobacterium tuberculosis in the search for novel antimycobacterial agents. Natural products constitute an important source of new drugs, and design and implementation of antimycobacterial susceptibility testing methods are necessary to evaluate the different extracts and compounds. In this study we have explored the antimycobacterial properties of 50 ethanolic extracts from different parts of 46 selected medicinal plants traditionally used in Sudan to treat infectious diseases. Materials and methods: Plants were harvested and ethanolic extracts were prepared. For selected extracts, fractionation with hydrophilic and hydrophobic solvents was undertaken. A luminometry-based assay was used for determination of mycobacterial growth in broth cultures and inside primary human macrophages in the presence or absence of plant extracts and fractions of extracts. Cytotoxicity was also assessed for active fractions of plant extracts. Results: Of the tested extracts, three exhibited a significant inhibitory effect on an avirulent strain of Mycobacterium tubercluosis (H37Ra) at the initial screening doses (125 and 6.25 mu g/ml). These were bark and leaf extracts of Khaya senegalensis and the leaf extract of Rosmarinus officinalis L. Further fractions of these plant extracts were prepared with n-hexane, chloroform, ethyl acetate, n-butanol, ethanol and water, and the activity of these extracts was retained in hydrophobic fractions. Cytotoxicity assays revealed that the chloroform fraction of Khaya senegalensis bark was non-toxic to human monocyte-derived macrophages and other cell types at the concentrations used and hence, further analysis, including assessment of IC50 and intracellular activity was done with this fraction. Conclusion: These results encourage further investigations to identify the active compound(s) within the chloroform fraction of Khaya senegalensis bark. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Mycobacterium tuberculosis; Sudanese medicinal plants; Primary human macrophages; Luminescence reporter assay; Cytotoxicity assay
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-113785 (URN)10.1016/j.jep.2014.09.020 (DOI)000347022700016 ()25261689 (PubMedID)
Note

Funding Agencies|Ekhaga Foundation [2011-33]; Swedish Insitute

Available from: 2015-02-02 Created: 2015-01-30 Last updated: 2019-01-07
Andersson, H., Eklund, D., Ngoh, E., Persson, A., Andersson, B., Svensson, K., . . . Stendahl, O. (2014). Apoptotic neutrophils augment the inflammatory response to Mycobacterium tuberculosis infection in human macrophages. PLoS ONE, 9(7), e101514
Open this publication in new window or tab >>Apoptotic neutrophils augment the inflammatory response to Mycobacterium tuberculosis infection in human macrophages
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2014 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, no 7, p. e101514-Article in journal (Refereed) Published
Abstract [en]

Macrophages in the lung are the primary cells being infected by Mycobacterium tuberculosis (Mtb) during tuberculosis. Innate immune cells such as macrophages and neutrophils are first recruited to the site of infection, and mount the early immune protection against this intracellular pathogen. Neutrophils are short-lived cells and removal of apoptotic cells by resident macrophages is a key event in the resolution of inflammation and tissue repair. Such anti-inflammatory activity is not compatible with effective immunity to intracellular pathogens. We therefore investigated how uptake of apoptotic neutrophils by Mtb-activated human monocyte-derived macrophages modulates their function. We show that Mtb infection exerts a potent pro-inflammatory activation of human macrophages with enhanced gene activation and release of several cytokines (TNF, IL-1ß, IL-6, IL-18 and IL-10). This response was augmented by apoptotic neutrophils. Macrophages containing both Mtb and apoptotic cells showed a stronger cytokine expression than non-infected cells. The enhanced macrophage response is linked to apoptotic neutrophil-driven activation of the NLRP3 inflammasome and subsequent IL-1β signalling. We also demonstrate that apoptotic neutrophils not only modulate the inflammatory response, but also enhance the capacity of infected macrophages to control intracellular growth of virulent Mtb. Taken together, these results suggest a novel role for apoptotic neutrophils in the modulation of the macrophage-dependent inflammatory response, which can contribute to the early control of Mtb infection.

Place, publisher, year, edition, pages
PLoS, 2014
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-100888 (URN)10.1371/journal.pone.0101514 (DOI)000338637300054 ()
Available from: 2013-11-14 Created: 2013-11-14 Last updated: 2017-12-06Bibliographically approved
Eklund, D., Welin, A., Andersson, H., Verma, D., Söderkvist, P., Stendahl, O., . . . Lerm, M. (2014). Human gene variants linked to enhanced NLRP3 activity limit intramacrophage growth of Mycobacterium tuberculosis. The Journal of infectious diseases, 209(5), 749-753
Open this publication in new window or tab >>Human gene variants linked to enhanced NLRP3 activity limit intramacrophage growth of Mycobacterium tuberculosis
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2014 (English)In: The Journal of infectious diseases, ISSN 1537-6613, Vol. 209, no 5, p. 749-753Article in journal (Refereed) Published
Abstract [en]

Activation of the NLRP3 inflammasome and subsequent generation of IL-1β is initiated in macrophages upon recognition of several stimuli. In the present work, we show that gain-of-function gene variants of inflammasome components known to predispose individuals to inflammatory disorders have a host-protective role during infection with Mycobacterium tuberculosis. By isolation of macrophages from patients and healthy blood donors with genetic variants in NLRP3 and CARD8 and subsequently infecting the cells by virulent M. tuberculosis, we show that these gene variants, combined, are associated with increased control of bacterial growth in human macrophages.

Place, publisher, year, edition, pages
University of Chicago Press / Oxford University Press (OUP), 2014
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-100889 (URN)10.1093/infdis/jit572 (DOI)000331873700016 ()24158955 (PubMedID)
Available from: 2013-11-14 Created: 2013-11-14 Last updated: 2015-04-10Bibliographically approved
Raffetseder, J., Pienaar, E., Blomgran, R., Eklund, D., Brodin Patcha, V., Andersson, H., . . . Lerm, M. (2014). Replication Rates of Mycobacterium tuberculosis in Human Macrophages Do Not Correlate with Mycobacterial Antibiotic Susceptibility. PLoS ONE, 9(11), e112426
Open this publication in new window or tab >>Replication Rates of Mycobacterium tuberculosis in Human Macrophages Do Not Correlate with Mycobacterial Antibiotic Susceptibility
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2014 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, no 11, p. e112426-Article in journal (Refereed) Published
Abstract [en]

The standard treatment of tuberculosis (TB) takes six to nine months to complete and this lengthy therapy contributes to the emergence of drug-resistant TB. TB is caused by Mycobacterium tuberculosis (Mtb) and the ability of this bacterium to switch to a dormant phenotype has been suggested to be responsible for the slow clearance during treatment. A recent study showed that the replication rate of a non-virulent mycobacterium, Mycobacterium smegmatis, did not correlate with antibiotic susceptibility. However, the question whether this observation also holds true for Mtb remains unanswered. Here, in order to mimic physiological conditions of TB infection, we established a protocol based on long-term infection of primary human macrophages, featuring Mtb replicating at different rates inside the cells. During conditions that restricted Mtb replication, the bacterial phenotype was associated with reduced acid-fastness. However, these phenotypically altered bacteria were as sensitive to isoniazid, pyrazinamide and ethambutol as intracellularly replicating Mtb. In support of the recent findings with M. smegmatis, we conclude that replication rates of Mtb do not correlate with antibiotic tolerance.

Place, publisher, year, edition, pages
Public Library of Science, 2014
National Category
Clinical Medicine Basic Medicine
Identifiers
urn:nbn:se:liu:diva-113014 (URN)10.1371/journal.pone.0112426 (DOI)000345250400061 ()25386849 (PubMedID)
Note

Funding Agencies|Bill and Melinda Gates Foundation; Swedish Research Council [2009-3821, 2012-3349]; Swedish International Development Cooperation Agency; Swedish Heart-Lung Foundation; King Oscar II Foundation; Carl Trygger Foundation; Clas Groschinsky Foundation

Available from: 2015-01-12 Created: 2015-01-08 Last updated: 2018-01-11
Andersson, H., Steel, D., Asp, J., Dahlenborg, K., Jonsson, M., Jeppsson, A., . . . Mandenius, C.-F. (2010). Assaying cardiac biomarkers for toxicity testing using biosensing and cardiomyocytes derived from human embryonic stem cells. JOURNAL OF BIOTECHNOLOGY, 150(1), 175-181
Open this publication in new window or tab >>Assaying cardiac biomarkers for toxicity testing using biosensing and cardiomyocytes derived from human embryonic stem cells
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2010 (English)In: JOURNAL OF BIOTECHNOLOGY, ISSN 0168-1656, Vol. 150, no 1, p. 175-181Article in journal (Refereed) Published
Abstract [en]

Human embryonic stem cell (hESC) derived cardiomyocytes are in the present study being used for testing drug-induced cardiotoxicity in a biosensor set-up. The design of an in vitro testing alternative provides a novel opportunity to surpass previous methods based on rodent cells or cell lines due to its significantly higher toxicological relevance. In this report we demonstrate how hESC-derived cardiomyocytes release detectable levels of two clinically decisive cardiac biomarkers, cardiac troponin T and fatty acid binding protein 3, when the cardiac cells are exposed to the well-known cardioactive drug compound. doxorubicin. The release is monitored by the immuno-biosensor technique surface plasmon resonance, particularly appropriate due to its capacity for parallel and high-throughput analysis in complex media.

Place, publisher, year, edition, pages
Elsevier Science B.V., Amsterdam., 2010
Keywords
In vitro toxicity testing, hESC-derived cardiomyocytes, Doxorubicin, Biosensors, Surface plasmon resonance. SPR
National Category
Engineering and Technology
Identifiers
urn:nbn:se:liu:diva-62153 (URN)10.1016/j.jbiotec.2010.06.023 (DOI)000283693600025 ()
Available from: 2010-11-19 Created: 2010-11-19 Last updated: 2019-01-22
Andersson, H., Kågedal, B. & Mandenius, C.-F. (2010). Monitoring of troponin release from cardiomyocytes during exposure to toxic substances using surface plasmon resonance biosensing. ANALYTICAL AND BIOANALYTICAL CHEMISTRY, 398(3), 1395-1402
Open this publication in new window or tab >>Monitoring of troponin release from cardiomyocytes during exposure to toxic substances using surface plasmon resonance biosensing
2010 (English)In: ANALYTICAL AND BIOANALYTICAL CHEMISTRY, ISSN 1618-2642, Vol. 398, no 3, p. 1395-1402Article in journal (Refereed) Published
Abstract [en]

Troponin T (TnT) is a useful biomarker for studying drug-induced toxicity effects on cardiac cells. We describe how a surface plasmon resonance (SPR) biosensor was applied to monitor the release of TnT from active HL-1 cardiomyocytes in vitro when exposed to cardiotoxic substances. Two monoclonal human TnT antibodies were compared in the SPR immunosensor to analyse the TnT release. The detection limit of TnT was determined to be 30 ng/ml in a direct assay set-up and to be 10 ng/ml in a sandwich assay format. Exposure of the cardiomyocytes to doxorubicin, troglitazone, quinidine and cobalt chloride for periods of 6 and 24 h gave significant SPR responses, whereas substances with low toxicity showed insignificant effects (ascorbic acid, methotrexate). The SPR results were verified with a validated immunochemiluminescence method which showed a correlation of r(2)=0.790.

Place, publisher, year, edition, pages
Springer Science Business Media, 2010
Keywords
Surface plasmon resonance, Troponin T, Cardiotoxicity, In vitro toxicity, HL-1 cardiomyocytes, Cytotoxicity screening
National Category
Engineering and Technology
Identifiers
urn:nbn:se:liu:diva-59731 (URN)10.1007/s00216-010-4041-9 (DOI)000281670400026 ()
Note

The original publication is available at www.springerlink.com: Henrik Andersson, Bertil Kågedal and Carl-Fredrik Mandenius, Monitoring of troponin release from cardiomyocytes during exposure to toxic substances using surface plasmon resonance biosensing, 2010, ANALYTICAL AND BIOANALYTICAL CHEMISTRY, (398), 3, 1395-1402. http://dx.doi.org/10.1007/s00216-010-4041-9 Copyright: Springer Science Business Media http://www.springerlink.com/

Available from: 2010-09-24 Created: 2010-09-24 Last updated: 2019-01-22
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