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  1. Article ; Online: A pulmonary endothelial amplification loop aggravates ex-vivo transfusion-related acute lung injury via increased toll-like receptor 4 and intra-cellular adhesion molecule-1 expression.

    Morsing, Sofia K H / Zeeuw van der Laan, Eveline / van Stalborch, Annemarieke D / van Buul, Jaap D / Kapur, Rick / Vlaar, Alexander P

    Transfusion

    2022  Volume 62, Issue 10, Page(s) 1961–1966

    Abstract: Background: Transfusion-Related Acute Lung Injury (TRALI) is a life-threatening complication of blood transfusions characterized by pulmonary endothelial cell damage and edema, with a high incidence in critically ill patients. The pathophysiology of ... ...

    Abstract Background: Transfusion-Related Acute Lung Injury (TRALI) is a life-threatening complication of blood transfusions characterized by pulmonary endothelial cell damage and edema, with a high incidence in critically ill patients. The pathophysiology of TRALI is unresolved, but can generally be hypothesized to follow a 2-hit model in which the first hit is elicited by the underlying clinical condition of the patient (e.g., inflammation, which can be reflected by LPS in experimental models), and the second hit is delivered by the blood transfusion product (e.g., HLA class I antibodies). Here, we report a synergistic role for LPS and HLA class I antibody binding to pulmonary endothelium resulting in enhanced inflammatory responses.
    Materials and methods: Pulmonary endothelial cells were treated with PBS or low-dose LPS, exclusively or in combination with anti-HLA class I. Endothelial surface expression of HLA class I, TLR4, and inflammatory marker ICAM-1 were measured, and trans-endothelial migration (TEM) of neutrophils was investigated.
    Results: LPS treatment of pulmonary endothelium enhanced HLA class I antibody binding, and combined LPS and HLA class I antibody binding enhanced TLR4 (LPS receptor) and ICAM-1 expression on the endothelial cell surface. Low-dose LPS and HLA antibody together also increased neutrophil TEM under physiological flow by on average 5-fold.
    Conclusion: We conclude that LPS and anti-HLA class I antibody have the ability to activate the pulmonary endothelium into a spiral of increasing inflammation, opening the opportunity to potentially block TLR4 to prevent or reduce the severity of TRALI in vivo.
    MeSH term(s) Endothelial Cells ; Endothelium ; Humans ; Inflammation ; Intercellular Adhesion Molecule-1 ; Lipopolysaccharide Receptors ; Lipopolysaccharides/pharmacology ; Toll-Like Receptor 4 ; Transfusion Reaction ; Transfusion-Related Acute Lung Injury/etiology
    Chemical Substances Lipopolysaccharide Receptors ; Lipopolysaccharides ; Toll-Like Receptor 4 ; Intercellular Adhesion Molecule-1 (126547-89-5)
    Language English
    Publishing date 2022-08-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 208417-x
    ISSN 1537-2995 ; 0041-1132
    ISSN (online) 1537-2995
    ISSN 0041-1132
    DOI 10.1111/trf.17076
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Endothelial cells of pulmonary origin display unique sensitivity to the bacterial endotoxin lipopolysaccharide.

    Morsing, Sofia K H / Zeeuw van der Laan, Eveline / van Stalborch, Anne-Marieke D / van Buul, Jaap D / Vlaar, Alexander P J / Kapur, Rick

    Physiological reports

    2022  Volume 10, Issue 8, Page(s) e15271

    Abstract: Acute respiratory distress syndrome (ARDS) is a major clinical problem without available therapies. Known risks for ARDS include severe sepsis, SARS-CoV-2, gram-negative bacteria, trauma, pancreatitis, and blood transfusion. During ARDS, blood fluids and ...

    Abstract Acute respiratory distress syndrome (ARDS) is a major clinical problem without available therapies. Known risks for ARDS include severe sepsis, SARS-CoV-2, gram-negative bacteria, trauma, pancreatitis, and blood transfusion. During ARDS, blood fluids and inflammatory cells enter the alveoli, preventing oxygen exchange from air into blood vessels. Reduced pulmonary endothelial barrier function, resulting in leakage of plasma from blood vessels, is one of the major determinants in ARDS. It is, however, unknown why systemic inflammation particularly targets the pulmonary endothelium, as endothelial cells (ECs) line all vessels in the vascular system of the body. In this study, we examined ECs of pulmonary, umbilical, renal, pancreatic, and cardiac origin for upregulation of adhesion molecules, ability to facilitate neutrophil (PMN) trans-endothelial migration (TEM) and for endothelial barrier function, in response to the gram-negative bacterial endotoxin LPS. Interestingly, we found that upon LPS stimulation, pulmonary ECs showed increased levels of adhesion molecules, facilitated more PMN-TEM and significantly perturbed the endothelial barrier, compared to other types of ECs. These observations could partly be explained by a higher expression of the adhesion molecule ICAM-1 on the pulmonary endothelial surface compared to other ECs. Moreover, we identified an increased expression of Cadherin-13 in pulmonary ECs, for which we demonstrated that it aids PMN-TEM in pulmonary ECs stimulated with LPS. We conclude that pulmonary ECs are uniquely sensitive to LPS, and intrinsically different, compared to ECs from other vascular beds. This may add to our understanding of the development of ARDS upon systemic inflammation.
    MeSH term(s) COVID-19 ; Cell Adhesion Molecules/metabolism ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; Humans ; Inflammation/metabolism ; Lipopolysaccharides/metabolism ; Lipopolysaccharides/pharmacology ; Respiratory Distress Syndrome ; SARS-CoV-2
    Chemical Substances Cell Adhesion Molecules ; Lipopolysaccharides
    Language English
    Publishing date 2022-05-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15271
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Update on the pathophysiology of transfusion-related acute lung injury.

    Zeeuw van der Laan, Eveline A N / van der Velden, Saskia / Porcelijn, Leendert / Semple, John W / van der Schoot, C Ellen / Kapur, Rick

    Current opinion in hematology

    2020  Volume 27, Issue 6, Page(s) 386–391

    Abstract: Purpose of review: The aim of this study was to discuss recent advances regarding the pathogenesis of transfusion-related acute lung injury (TRALI), which highlight the pathogenic role of macrophages.: Recent findings: TRALI remains a leading cause ... ...

    Abstract Purpose of review: The aim of this study was to discuss recent advances regarding the pathogenesis of transfusion-related acute lung injury (TRALI), which highlight the pathogenic role of macrophages.
    Recent findings: TRALI remains a leading cause of transfusion-related fatalities, despite the success of the mitigation strategy, and therapeutic approaches are unavailable. Neutrophils (PMNs) are recognized pathogenic cells in TRALI. Macrophages have previously also been suggested to be pathogenic in mice via binding of C5a to their C5a-receptor, producing reactive oxygen species (ROS), which damages the pulmonary endothelium. Recent work has further highlighted the role of macrophages in the TRALI-pathogenesis. It has been shown that the protein osteopontin (OPN) released by macrophages is critical for pulmonary PMN recruitment in mice suffering from TRALI and that targeting OPN prevents the occurrence of TRALI. Another recent study demonstrated the importance of M1-polarized alveolar macrophages in murine TRALI induction by showing that α1-antitrypsin (AAT) overexpression prevented TRALI in mice through decreasing the polarization of alveolar macrophages towards the M1 phenotype.
    Summary: Apart from PMNs, macrophages also appear to be important in the pathogenesis of TRALI. Targeting the pathogenic functions of macrophages may be a promising therapeutic strategy to explore in TRALI.
    Language English
    Publishing date 2020-08-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1153887-9
    ISSN 1531-7048 ; 1065-6251
    ISSN (online) 1531-7048
    ISSN 1065-6251
    DOI 10.1097/MOH.0000000000000607
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3703: Show issues Location:
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  4. Article ; Online: Evaluation of Platelet Responses in Transfusion-Related Acute Lung Injury (TRALI).

    Zeeuw van der Laan, Eveline A N / van der Velden, Saskia / Porcelijn, Leendert / Semple, John W / van der Schoot, C Ellen / Kapur, Rick

    Transfusion medicine reviews

    2020  Volume 34, Issue 4, Page(s) 227–233

    Abstract: Platelets are versatile cells which are capable of eliciting nonhemostatic immune functions, especially under inflammatory conditions. Depending on the specific setting, platelets may be either protective or pathogenic in acute lung injury and acute ... ...

    Abstract Platelets are versatile cells which are capable of eliciting nonhemostatic immune functions, especially under inflammatory conditions. Depending on the specific setting, platelets may be either protective or pathogenic in acute lung injury and acute respiratory distress syndrome (ARDS). Their role in transfusion-related acute lung injury (TRALI) is less well defined; however, it has been hypothesized that recipient platelets and transfused platelets both play a pathogenic role in TRALI. Overall, despite conflicting findings, it appears that recipient platelets may play a pathogenic role in antibody-mediated TRALI; however, their contribution appears to be limited. It is imperative to first validate the involvement of recipient platelets by standardizing the animal models, methods, reagents, and readouts for lung injury and taking the animal housing environment into consideration. For the involvement of transfused platelets in TRALI, it appears that predominantly lipids such as ceramide in stored platelets are able to induce TRALI in animal models. These studies will also need to be validated, and moreover, the platelet-derived lipid-mediated mechanisms leading to TRALI will need to be investigated.
    MeSH term(s) Animals ; Blood Platelets/immunology ; Humans ; Platelet Transfusion/adverse effects ; Platelet Transfusion/methods ; Transfusion-Related Acute Lung Injury/etiology ; Transfusion-Related Acute Lung Injury/immunology ; Transfusion-Related Acute Lung Injury/physiopathology
    Keywords covid19
    Language English
    Publishing date 2020-09-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639107-2
    ISSN 1532-9496 ; 0887-7963
    ISSN (online) 1532-9496
    ISSN 0887-7963
    DOI 10.1016/j.tmrv.2020.08.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2239: Show issues Location:
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  5. Article ; Online: Biological and structural characterization of murine TRALI antibody reveals increased Fc-mediated complement activation.

    Zeeuw van der Laan, Eveline A N / van der Velden, Saskia / Bentlage, Arthur E H / Larsen, Mads D / van Osch, Thijs L J / Mok, Juk Yee / Brasser, Giso / Geerdes, Dionne M / Koeleman, Carolien A M / Nouta, Jan / Semple, John W / Porcelijn, Leendert / van Esch, Wim J E / Wuhrer, Manfred / van der Schoot, C Ellen / Vidarsson, Gestur / Kapur, Rick

    Blood advances

    2020  Volume 4, Issue 16, Page(s) 3875–3885

    Abstract: Transfusion-related acute lung injury (TRALI) remains a leading cause of transfusion-related deaths. In most cases, anti-leukocyte antibodies in the transfusion product trigger TRALI, but not all anti-leukocyte antibodies cause TRALI. It has been shown ... ...

    Abstract Transfusion-related acute lung injury (TRALI) remains a leading cause of transfusion-related deaths. In most cases, anti-leukocyte antibodies in the transfusion product trigger TRALI, but not all anti-leukocyte antibodies cause TRALI. It has been shown that the anti-major histocompatibility complex (MHC) class I antibody 34-1-2S (anti-H-2Kd) causes TRALI in BALB/c mice (MHC class I haplotype H-2Kd), whereas SF1.1.10 (anti-H-2Kd) does not. In C57BL/6 mice (MHC class I haplotype H-2Kb), TRALI only occurs when anti-MHC class I antibody AF6-88.5.5.3 (anti-H-2Kb) is administered together with a high dose of 34-1-2S. It remains unknown which specific antibody characteristics are responsible for eliciting TRALI. We therefore investigated several biological and structural features of 34-1-2S compared with other anti-MHC class I antibodies, which on their own do not cause TRALI: SF1.1.10 and AF6-88.5.5.3. No substantial differences were observed between the TRALI-causing 34-1-2S and the TRALI-resistant SF1.1.10 regarding binding affinity to H-2Kd. Regarding binding affinity to H-2Kb, only AF6-88.5.5.3 potently bound to H-2Kb, whereas 34-1-2S exhibited weak but significant cross-reactivity. Furthermore, the binding affinity to FcγRs as well as the Fc glycan composition seemed to be similar for all antibodies. Similar Fc glycosylation profiles were also observed for human TRALI-causing donor anti-HLA antibodies compared with human anti-HLA antibodies from control donors. 34-1-2S, however, displayed superior complement activation capacity, which was fully Fc dependent and not significantly dependent on Fc glycosylation. We conclude that TRALI induction is not correlated with Fab- and Fc-binding affinities for antigen and FcγRs, respectively, nor with the composition of Fc glycans; but increased Fc-mediated complement activation is correlated with TRALI induction.
    MeSH term(s) Animals ; Complement Activation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Transfusion Reaction ; Transfusion-Related Acute Lung Injury
    Language English
    Publishing date 2020-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2020002291
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    Zs.A 7153: Show issues Location:
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  6. Article ; Online: Impact of hypoxia on chemoresistance of mesothelioma mediated by the proton-coupled folate transporter, and preclinical activity of new anti-LDH-A compounds.

    Li Petri, Giovanna / El Hassouni, Btissame / Sciarrillo, Rocco / Funel, Niccola / Mantini, Giulia / Zeeuw van der Laan, Eveline A / Cascioferro, Stella / Avan, Amir / Zucali, Paolo Andrea / Zaffaroni, Nadia / Lagerweij, Tonny / Parrino, Barbara / Smid, Kees / Deraco, Marcello / Granchi, Carlotta / Braczko, Alicja / Smolenski, Ryszard T / Matherly, Larry H / Jansen, Gerrit /
    Assaraf, Yehuda G / Diana, Patrizia / Cloos, Jacqueline / Peters, Godefridus J / Minutolo, Filippo / Giovannetti, Elisa

    British journal of cancer

    2020  Volume 123, Issue 4, Page(s) 644–656

    Abstract: Background: Expression of proton-coupled folate transporter (PCFT) is associated with survival of mesothelioma patients treated with pemetrexed, and is reduced by hypoxia, prompting studies to elucidate their correlation.: Methods: Modulation of ... ...

    Abstract Background: Expression of proton-coupled folate transporter (PCFT) is associated with survival of mesothelioma patients treated with pemetrexed, and is reduced by hypoxia, prompting studies to elucidate their correlation.
    Methods: Modulation of glycolytic gene expression was evaluated by PCR arrays in tumour cells and primary cultures growing under hypoxia, in spheroids and after PCFT silencing. Inhibitors of lactate dehydrogenase (LDH-A) were tested in vitro and in vivo. LDH-A expression was determined in tissue microarrays of radically resected malignant pleural mesothelioma (MPM, N = 33) and diffuse peritoneal mesothelioma (DMPM, N = 56) patients.
    Results: Overexpression of hypoxia marker CAIX was associated with low PCFT expression and decreased MPM cell growth inhibition by pemetrexed. Through integration of PCR arrays in hypoxic cells and spheroids and following PCFT silencing, we identified the upregulation of LDH-A, which correlated with shorter survival of MPM and DMPM patients. Novel LDH-A inhibitors enhanced spheroid disintegration and displayed synergistic effects with pemetrexed in MPM and gemcitabine in DMPM cells. Studies with bioluminescent hypoxic orthotopic and subcutaneous DMPM athymic-mice models revealed the marked antitumour activity of the LDH-A inhibitor NHI-Glc-2, alone or combined with gemcitabine.
    Conclusions: This study provides novel insights into hypoxia/PCFT-dependent chemoresistance, unravelling the potential prognostic value of LDH-A, and demonstrating the preclinical activity of LDH-A inhibitors.
    MeSH term(s) Animals ; Antigens, Neoplasm/genetics ; Antigens, Neoplasm/metabolism ; Carbonic Anhydrase IX/genetics ; Carbonic Anhydrase IX/metabolism ; Cell Culture Techniques ; Cell Hypoxia ; Cell Line, Tumor ; Deoxycytidine/administration & dosage ; Deoxycytidine/analogs & derivatives ; Deoxycytidine/pharmacology ; Drug Resistance, Neoplasm/drug effects ; Drug Synergism ; Enzyme Inhibitors/administration & dosage ; Enzyme Inhibitors/pharmacology ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; L-Lactate Dehydrogenase/genetics ; Mesothelioma, Malignant/drug therapy ; Mesothelioma, Malignant/genetics ; Mesothelioma, Malignant/metabolism ; Mice ; Pemetrexed/administration & dosage ; Pemetrexed/pharmacology ; Peritoneal Neoplasms/drug therapy ; Peritoneal Neoplasms/genetics ; Peritoneal Neoplasms/metabolism ; Pleural Neoplasms/drug therapy ; Pleural Neoplasms/genetics ; Pleural Neoplasms/metabolism ; Proton-Coupled Folate Transporter/genetics ; Proton-Coupled Folate Transporter/metabolism ; Xenograft Model Antitumor Assays
    Chemical Substances Antigens, Neoplasm ; Enzyme Inhibitors ; Proton-Coupled Folate Transporter ; SLC46A1 protein, human ; Pemetrexed (04Q9AIZ7NO) ; Deoxycytidine (0W860991D6) ; gemcitabine (B76N6SBZ8R) ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; LDHA protein, human (EC 1.1.1.27) ; CA9 protein, human (EC 4.2.1.1) ; Carbonic Anhydrase IX (EC 4.2.1.1)
    Language English
    Publishing date 2020-06-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80075-2
    ISSN 1532-1827 ; 0007-0920
    ISSN (online) 1532-1827
    ISSN 0007-0920
    DOI 10.1038/s41416-020-0912-9
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  7. Article ; Online: Splicing modulation as novel therapeutic strategy against diffuse malignant peritoneal mesothelioma.

    Sciarrillo, Rocco / Wojtuszkiewicz, Anna / El Hassouni, Btissame / Funel, Niccola / Gandellini, Paolo / Lagerweij, Tonny / Buonamici, Silvia / Blijlevens, Maxime / Zeeuw van der Laan, Eveline A / Zaffaroni, Nadia / Deraco, Marcello / Kusamura, Shigeki / Würdinger, Tom / Peters, Godefridus J / Molthoff, Carla F M / Jansen, Gerrit / Kaspers, Gertjan J L / Cloos, Jacqueline / Giovannetti, Elisa

    EBioMedicine

    2018  Volume 39, Page(s) 215–225

    Abstract: Introduction: Therapeutic options for diffuse malignant peritoneal mesothelioma (DMPM) are limited to surgery and locoregional chemotherapy. Despite improvements in survival rates, patients eventually succumb to disease progression. We investigated ... ...

    Abstract Introduction: Therapeutic options for diffuse malignant peritoneal mesothelioma (DMPM) are limited to surgery and locoregional chemotherapy. Despite improvements in survival rates, patients eventually succumb to disease progression. We investigated splicing deregulation both as molecular prognostic factor and potential novel target in DMPM, while we tested modulators of SF3b complex for antitumor activity.
    Methods: Tissue-microarrays of 64 DMPM specimens were subjected to immunohistochemical assessment of SF3B1 expression and correlation to clinical outcome. Two primary cell cultures were used for gene expression profiling and in vitro screening of SF3b modulators. Drug-induced splicing alterations affecting downstream cellular pathways were detected through RNA sequencing. Ultimately, we established bioluminescent orthotopic mouse models to test the efficacy of splicing modulation in vivo.
    Results: Spliceosomal genes are differentially upregulated in DMPM cells compared to normal tissues and high expression of SF3B1 correlated with poor clinical outcome in univariate and multivariate analysis. SF3b modulators (Pladienolide-B, E7107, Meayamycin-B) showed potent cytotoxic activity in vitro with IC50 values in the low nanomolar range. Differential splicing analysis of Pladienolide-B-treated cells revealed abundant alterations of transcripts involved in cell cycle, apoptosis and other oncogenic pathways. This was validated by RT-PCR and functional assays. E7107 demonstrated remarkable in vivo antitumor efficacy, with significant improvement of survival rates compared to vehicle-treated controls.
    Conclusions: SF3B1 emerged as a novel potential prognostic factor in DMPM. Splicing modulators markedly impair cancer cell viability, resulting also in potent antitumor activity in vivo. Our data designate splicing as a promising therapeutic target in DMPM.
    MeSH term(s) Aged ; Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Epoxy Compounds/administration & dosage ; Epoxy Compounds/pharmacology ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks/drug effects ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Macrolides/administration & dosage ; Macrolides/pharmacology ; Male ; Mesothelioma/drug therapy ; Mesothelioma/genetics ; Mesothelioma/metabolism ; Mesothelioma, Malignant ; Mice ; Middle Aged ; Morpholines/administration & dosage ; Morpholines/pharmacology ; Peritoneal Neoplasms/drug therapy ; Peritoneal Neoplasms/genetics ; Peritoneal Neoplasms/metabolism ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Pyrans/administration & dosage ; Pyrans/pharmacology ; RNA Splicing/drug effects ; RNA Splicing Factors/genetics ; RNA Splicing Factors/metabolism ; Tissue Array Analysis/methods ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents ; E 7107 ; Epoxy Compounds ; Macrolides ; Morpholines ; Phosphoproteins ; Pyrans ; RNA Splicing Factors ; SF3B1 protein, human ; meayamycin B ; pladienolide B
    Language English
    Publishing date 2018-12-20
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2018.12.025
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