7 results on '"Henriksen, Katerina Nezvalova"'
Search Results
2. CXCL16 associates with adverse outcome and cardiac involvement in hospitalized patients with Covid-19
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Gregersen, Ida, primary, Ueland, Thor, additional, Holter, Jan Cato, additional, Olsen, Maria Belland, additional, Michelsen, Annika E, additional, Murphy, Sarah L, additional, Tveita, Anders Aune, additional, Henriksen, Katerina Nezvalova, additional, Hoel, Hedda, additional, Nordberg, Lena Bugge, additional, Holten, Aleksander Rygh, additional, Edvardsen, Thor, additional, Yang, Kuan, additional, Heggelund, Lars, additional, Trøseid, Marius, additional, Müller, Fredrik, additional, Kildal, Anders Benjamin, additional, Dyrhol-Riise, Anne Ma, additional, Barratt-Due, Andreas, additional, Dahl, Tuva B, additional, Aukrust, Pål, additional, and Halvorsen, Bente, additional
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- 2022
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3. High circulating levels of the homeostatic chemokines CCL19 and CCL21 predict mortality and disease severity in Covid-19
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Tveita, Anders, Murphy, Sarah Louise, Holter, Jan Cato, Kildal, Anders Benjamin, Michelsen, Annika E, Lerum, Tøri Vigeland, Kaarbø, Mari, Heggelund, Lars, Holten, Aleksander Rygh, Finbråten, Ane-Kristine, Müller, Karl Erik, Mathiessen, Alexander, Bøe, Simen, Fevang, Børre, Granerud, Beathe Kiland, Tonby, Kristian, Lind, Andreas, Dudman, Susanne Gjeruldsen, Henriksen, Katerina Nezvalova, Müller, Fredrik, Skjønsberg, Ole Henning, Trøseid, Marius, Barratt-Due, Andreas, Dyrhol-Riise, Anne Ma, Aukrust, Pål, Halvorsen, Bente, Dahl, Tuva Børresdatter, Ueland, Thor, Austad, Cathrine, Bogen, Mette, Hermann, Anne, Opsand, Hanne, Steinsvik, Trude, Woll, Bjørn Martin, Christensen, Erik Egeland, Eftestøl, Kristin, Hesstvedt, Liv, Jenum, Synne, Jørgensen, Marthe Jøntvedt, Landaas, Elisabeth Toverud, Nur, Sarah, Ormaasen, Vidar, Pettersen, Frank Olav, Quist-Paulsen, Else, Reikvam, Dag Henrik, Røstad, Kjerstin, Skeie, Linda, Steffensen, Anne Katrine, Stiksrud, Birgitte, Gravrok, Berit, Skogen, Vegard, Tylden, Garth Daryl, Andersen, Jan Terje, Kolderup, Anette, Kåsine, Trine, Lund-Johansen, Fridtjof, Olsen, Inge Christoffer, Skåra, Karoline Hansen, Tran, Trung, Fladeby, Cathrine, Holberg-Petersen, Mona, Johal, Simreen Kaur, Vaage, Eline Brenno, Aballi, Saad, Brynhildsen, Jorunn, Ghanima, Waleed, Halstensen, Anne Marie, Berg, Åse, Blomberg, Bjørn, Kvåle, Reidar, Langeland, Nina, Mohn, Kristin Greve Isdahl, Dalgard, Olav, Eiken, Ragnhild, Molvik, Richard Alexander, Ystrøm, Carl Magnus, Ernst, Gernot, Thoresen, Lars, Gustad, Lise Tuset, Saxhaug, Lars Mølgaard, Skei, Nina Vibeche, Hannula, Raisa, Haugli, Mette, Olsen, Roy Bjørkholt, Hoel, Hedda, Hoff, Dag Arne Lihaug, Johannessen, Asgeir, Åsheim-Hansen, Bjørn, Kittang, Bård Reikvam, Le, Lan Ai Kieu, Manotheepan, Ravinea, Nordberg, Lena Bugge, Rasmussen, Hans Schmidt, Stenvik, Grethe-Elisabeth, Thorkildsen, Ruth Foseide, Vinge, Leif Erik, Mielnik, Pawel, Skudal, Hilde, and Tholin, Birgitte
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Inflammation ,Receptors, CCR7 ,Infectious Diseases ,Chemokine CCL21 ,SARS-CoV-2 ,Patient Acuity ,Humans ,Chemokine CCL19 ,COVID-19 ,Immunology and Allergy ,Chemokines - Abstract
Background Immune dysregulation is a major factor in the development of severe coronavirus disease 2019 (COVID-19). The homeostatic chemokines CCL19 and CCL21 have been implicated as mediators of tissue inflammation, but data on their regulation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is limited. We thus investigated the levels of these chemokines in COVID-19 patients. Methods Serial blood samples were obtained from patients hospitalized with COVID-19 (n = 414). Circulating CCL19 and CCL21 levels during hospitalization and 3-month follow-up were analyzed. In vitro assays and analysis of RNAseq data from public repositories were performed to further explore possible regulatory mechanisms. Results A consistent increase in circulating levels of CCL19 and CCL21 was observed, with high levels correlating with disease severity measures, including respiratory failure, need for intensive care, and 60-day all-cause mortality. High levels of CCL21 at admission were associated with persisting impairment of pulmonary function at the 3-month follow-up. Conclusions Our findings highlight CCL19 and CCL21 as markers of immune dysregulation in COVID-19. This may reflect aberrant regulation triggered by tissue inflammation, as observed in other chronic inflammatory and autoimmune conditions. Determination of the source and regulation of these chemokines and their effects on lung tissue is warranted to further clarify their role in COVID-19. Clinical Trials Registration NCT04321616 and NCT04381819.
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- 2022
4. Gut microbiota alterations in patients with persistent respiratory dysfunction three months after severe COVID-19
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Vestad, Beate, primary, Ueland, Thor, additional, Lerum, Tøri Vigeland, additional, Børresdatter Dahl, Tuva, additional, Holm, Kristian, additional, Barratt-Due, Andreas, additional, Kåsine, Trine, additional, Dyrhol-Riise, Anne Ma, additional, Stiksrud, Birgitte, additional, Tonby, Kristian, additional, Hoel, Hedda, additional, Olsen, Inge Christoffer, additional, Henriksen, Katerina Nezvalova, additional, Tveita, Anders, additional, Manotheepan, Ravinea, additional, Haugli, Mette, additional, Eiken, Ragnhild, additional, Berg, Åse, additional, Halvorsen, Bente, additional, Lekva, Tove, additional, Ranheim, Trine, additional, Michelsen, Annika Elisabeth, additional, Kildal, Anders Benjamin, additional, Johannessen, Asgeir, additional, Thoresen, Lars, additional, Skudal, Hilde, additional, Kittang, Bård Reiakvam, additional, Bjørkholt Olsen, Roy, additional, Ystrøm, Carl Magnus, additional, Skei, Nina Vibeche, additional, Hannula, Raisa, additional, Aballi, Saad, additional, Kvåle, Reidar, additional, Skjønsberg, Ole Henning, additional, Aukrust, Pål, additional, Hov, Johannes Roksund, additional, and Trøseid, Marius, additional
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- 2021
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5. Respiratory dysfunction three months after severe COVID‐19 is associated with gut microbiota alterations.
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Vestad, Beate, Ueland, Thor, Lerum, Tøri Vigeland, Dahl, Tuva Børresdatter, Holm, Kristian, Barratt‐Due, Andreas, Kåsine, Trine, Dyrhol‐Riise, Anne Ma, Stiksrud, Birgitte, Tonby, Kristian, Hoel, Hedda, Olsen, Inge Christoffer, Henriksen, Katerina Nezvalova, Tveita, Anders, Manotheepan, Ravinea, Haugli, Mette, Eiken, Ragnhild, Berg, Åse, Halvorsen, Bente, and Lekva, Tove
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CORONAVIRUS diseases ,GUT microbiome ,POST-acute COVID-19 syndrome ,COVID-19 ,LUNG volume measurements ,CARBON monoxide - Abstract
Background: Although coronavirus disease 2019 (COVID‐19) is primarily a respiratory infection, mounting evidence suggests that the gastrointestinal tract is involved in the disease, with gut barrier dysfunction and gut microbiota alterations being related to disease severity. Whether these alterations persist and are related to long‐term respiratory dysfunction remains unknown. Methods: Plasma was collected during hospital admission and after 3 months from the NOR‐Solidarity trial (n = 181) and analyzed for markers of gut barrier dysfunction and inflammation. At the 3‐month follow‐up, pulmonary function was assessed by measuring the diffusing capacity of the lungs for carbon monoxide (DLCO). Rectal swabs for gut microbiota analyses were collected (n = 97) and analyzed by sequencing the 16S rRNA gene. Results: Gut microbiota diversity was reduced in COVID‐19 patients with respiratory dysfunction, defined as DLCO below the lower limit of normal 3 months after hospitalization. These patients also had an altered global gut microbiota composition, with reduced relative abundance of 20 bacterial taxa and increased abundance of five taxa, including Veillonella, potentially linked to fibrosis. During hospitalization, increased plasma levels of lipopolysaccharide‐binding protein (LBP) were strongly associated with respiratory failure, defined as pO2/fiO2 (P/F ratio) <26.6 kPa. LBP levels remained elevated during and after hospitalization and were associated with low‐grade inflammation and respiratory dysfunction after 3 months. Conclusion: Respiratory dysfunction after COVID‐19 is associated with altered gut microbiota and persistently elevated LBP levels. Our results should be regarded as hypothesis generating, pointing to a potential gut–lung axis that should be further investigated in relation to long‐term pulmonary dysfunction and long COVID. [ABSTRACT FROM AUTHOR]
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- 2022
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6. Evaluation of Remdesivir and Hydroxychloroquine on Viral Clearance in COVID-19 Patients: Results from the NOR-Solidarity Randomised Trial
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Barratt-Due, Andreas, primary, Olsen, Inge Christoffer, additional, Henriksen, Katerina Nezvalova, additional, Kåsine, Trine, additional, Lund-Johansen, Fridtjof, additional, Hoel, Hedda, additional, Holten, Aleksander Rygh, additional, Tveita, Anders, additional, Mathiessen, Alexander, additional, Haugli, Mette, additional, Eiken, Ragnhild, additional, Kildal, Anders Benjamin, additional, Berg, Åse, additional, Johannessen, Asgeir, additional, Heggelund, Lars, additional, Dahl, Tuva Børresdatter, additional, Skåra, Karoline Hansen, additional, Mielnik, Pawel, additional, Le, Lan Ai Kieu, additional, Thoresen, Lars, additional, Ernst, Gernot, additional, Hoff, Dag Arne Lihaug, additional, Skudal, Hilde, additional, Kittang, Bård Reiakvam, additional, Olsen, Roy Bjørkholt, additional, Tholin, Birgitte, additional, Ystrøm, Carl Magnus, additional, Skei, Nina Vibeche, additional, Tran, Trung, additional, Dudman, Susanne, additional, Andersen, Jan Terje, additional, Hannula, Raisa, additional, Dalgard, Olav, additional, Finbråten, Ane-Kristine, additional, Tonby, Kristian, additional, Blomberg, Bjørn, additional, Aballi, Saad, additional, Fladeby, Cathrine, additional, Steffensen, Anne, additional, Müller, Fredrik, additional, Dyrhol-Riise, Anne Ma, additional, Trøseid, Marius, additional, and Aukrust, Pål, additional
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- 2021
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- View/download PDF
7. High Circulating Levels of the Homeostatic Chemokines CCL19 and CCL21 Predict Mortality and Disease Severity in COVID-19.
- Author
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Tveita A, Murphy SL, Holter JC, Kildal AB, Michelsen AE, Lerum TV, Kaarbø M, Heggelund L, Holten AR, Finbråten AK, Müller KE, Mathiessen A, Bøe S, Fevang B, Granerud BK, Tonby K, Lind A, Dudman SG, Henriksen KN, Müller F, Skjønsberg OH, Trøseid M, Barratt-Due A, Dyrhol-Riise AM, Aukrust P, Halvorsen B, Dahl TB, and Ueland T
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- Humans, Chemokine CCL19, Chemokine CCL21, Chemokines, Inflammation, Patient Acuity, Receptors, CCR7, SARS-CoV-2, COVID-19
- Abstract
Background: Immune dysregulation is a major factor in the development of severe coronavirus disease 2019 (COVID-19). The homeostatic chemokines CCL19 and CCL21 have been implicated as mediators of tissue inflammation, but data on their regulation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is limited. We thus investigated the levels of these chemokines in COVID-19 patients., Methods: Serial blood samples were obtained from patients hospitalized with COVID-19 (n = 414). Circulating CCL19 and CCL21 levels during hospitalization and 3-month follow-up were analyzed. In vitro assays and analysis of RNAseq data from public repositories were performed to further explore possible regulatory mechanisms., Results: A consistent increase in circulating levels of CCL19 and CCL21 was observed, with high levels correlating with disease severity measures, including respiratory failure, need for intensive care, and 60-day all-cause mortality. High levels of CCL21 at admission were associated with persisting impairment of pulmonary function at the 3-month follow-up., Conclusions: Our findings highlight CCL19 and CCL21 as markers of immune dysregulation in COVID-19. This may reflect aberrant regulation triggered by tissue inflammation, as observed in other chronic inflammatory and autoimmune conditions. Determination of the source and regulation of these chemokines and their effects on lung tissue is warranted to further clarify their role in COVID-19., Clinical Trials Registration: NCT04321616 and NCT04381819., Competing Interests: Potential conflicts of interest. The authors: No reported conflicts of interest. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed., (© The Author(s) 2022. Published by Oxford University Press on behalf of Infectious Diseases Society of America.)
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- 2022
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