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  1. AU="Chen-Liaw, Alice"
  2. AU="Tywoniuk, K"
  3. AU="Nie, Zhiqiang"
  4. AU="Carlson, Jeffrey"
  5. AU="Yuan, Yunchang"
  6. AU="Russell"
  7. AU="Arnaud, Claire"
  8. AU="Quaranta, Marco"
  9. AU="Soltani, Farhad"
  10. AU="Cho, Ho-Seong"
  11. AU="Kuijer, Wietske"
  12. AU=Al-Atabany Walid AU=Al-Atabany Walid
  13. AU="Sundberg, Carl Johan"
  14. AU="Patel, Tushar"
  15. AU="Simgen, H."
  16. AU=Carter Henry Yates
  17. AU="Tangoulis, Vassilis"
  18. AU="Ma, Michelle"
  19. AU="Osuch, Isabelle"
  20. AU="Arora, Garhima"

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  1. Artikel ; Online: Immunoglobulin A antibody composition is sculpted to bind the self gut microbiome.

    Yang, Chao / Chen-Liaw, Alice / Spindler, Matthew P / Tortorella, Domenico / Moran, Thomas M / Cerutti, Andrea / Faith, Jeremiah J

    Science immunology

    2022  Band 7, Heft 73, Seite(n) eabg3208

    Abstract: Despite being the most abundantly secreted immunoglobulin isotype, the pattern of reactivity of immunoglobulin A (IgA) antibodies toward each individual's own gut commensal bacteria still remains elusive. By colonizing germ-free mice with defined ... ...

    Abstract Despite being the most abundantly secreted immunoglobulin isotype, the pattern of reactivity of immunoglobulin A (IgA) antibodies toward each individual's own gut commensal bacteria still remains elusive. By colonizing germ-free mice with defined commensal bacteria, we found that the binding specificity of bulk fecal and serum IgA toward resident gut bacteria resolves well at the species level and has modest strain-level specificity. IgA hybridomas generated from lamina propria B cells of gnotobiotic mice showed that most IgA clones recognized a single bacterial species, whereas a small portion displayed cross-reactivity. Orally administered hybridoma-produced IgAs still retained bacterial antigen binding capability, implying the potential for a new class of therapeutic antibodies. Species-specific IgAs had a range of strain specificities. Given the distinctive bacterial species and strain composition found in each individual's gut, our findings suggest the IgA antibody repertoire is shaped uniquely to bind "self" gut bacteria.
    Mesh-Begriff(e) Animals ; B-Lymphocytes ; Clone Cells ; Gastrointestinal Microbiome ; Hybridomas ; Immunoglobulin A ; Mice
    Chemische Substanzen Immunoglobulin A
    Sprache Englisch
    Erscheinungsdatum 2022-07-08
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abg3208
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Inhibition of exendin-4-induced steatosis by protein kinase A in cultured HepG2 human hepatoma cells.

    Chen-Liaw, Alice Y / Hammel, Gabrielle / Gomez, George

    In vitro cellular & developmental biology. Animal

    2017  Band 53, Heft 8, Seite(n) 721–727

    Abstract: Nonalcoholic fatty liver is characterized by the abnormal accumulation of triglycerides within hepatocytes, resulting in a steatotic liver. Glucagon-like peptide 1 and its analog exendin-4 can ameliorate certain aspects of this syndrome by inducing ... ...

    Abstract Nonalcoholic fatty liver is characterized by the abnormal accumulation of triglycerides within hepatocytes, resulting in a steatotic liver. Glucagon-like peptide 1 and its analog exendin-4 can ameliorate certain aspects of this syndrome by inducing weight loss and reducing hepatic triglyceride accumulation, but it is unclear whether these effects result from the effects of glucagon-like peptide 1 on the pancreas, or from direct action on the liver. This study investigated the direct action and putative cellular mechanism of exendin-4 on steatotic hepatocytes in culture. Steatosis was induced in cultured HepG2 human hepatoma cells by incubation in media supplemented with 2 mM each of linoleic acid and oleic acid. Steatotic hepatocytes were then pre-incubated in the protein kinase A inhibitor H89 for 30 min, then treated with exendin-4 over a period of 24 h. Cell viability and triglyceride content were characterized by a TUNEL assay and AdipoRed staining, respectively. Our results showed that steatotic cells maintained high levels of intracellular triglycerides (80%) compared to lean controls (25%). Exendin-4 treatment caused a significant reduction in intracellular triglyceride content after 12 h that persisted through 24 h, while protein kinase A inhibitors abolished the effects of exendin-4. The results demonstrate the exendin-4 induces a partial reduction in triglycerides in steatotic hepatocytes within 12 h via the GLP-1 receptor-mediated activation of protein kinase A. Thus, the reduction in hepatocyte triglyceride accumulation is likely driven primarily by downregulation of lipogenesis and upregulation of β-oxidation of free fatty acids.
    Mesh-Begriff(e) Carcinoma, Hepatocellular/chemically induced ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Survival/drug effects ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Fatty Liver/chemically induced ; Fatty Liver/drug therapy ; Fatty Liver/metabolism ; Fatty Liver/pathology ; Glucagon-Like Peptide 1/genetics ; Glucagon-Like Peptide 1/metabolism ; Hep G2 Cells ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Isoquinolines/administration & dosage ; Linoleic Acid/toxicity ; Lipogenesis/drug effects ; Lipogenesis/genetics ; Liver Neoplasms/chemically induced ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Oleic Acid/toxicity ; Pancreas/drug effects ; Pancreas/microbiology ; Peptides/administration & dosage ; Peptides/antagonists & inhibitors ; Peptides/metabolism ; Sulfonamides/administration & dosage ; Triglycerides/metabolism ; Venoms/administration & dosage ; Venoms/metabolism
    Chemische Substanzen Isoquinolines ; Peptides ; Sulfonamides ; Triglycerides ; Venoms ; Oleic Acid (2UMI9U37CP) ; Glucagon-Like Peptide 1 (89750-14-1) ; Linoleic Acid (9KJL21T0QJ) ; exenatide (9P1872D4OL) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide (M876330O56)
    Sprache Englisch
    Erscheinungsdatum 2017-09
    Erscheinungsland Germany
    Dokumenttyp Journal Article
    ZDB-ID 1077810-x
    ISSN 1543-706X ; 0883-8364 ; 1071-2690
    ISSN (online) 1543-706X
    ISSN 0883-8364 ; 1071-2690
    DOI 10.1007/s11626-017-0181-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Author Correction: Precise quantification of bacterial strains after fecal microbiota transplantation delineates long-term engraftment and explains outcomes.

    Aggarwala, Varun / Mogno, Ilaria / Li, Zhihua / Yang, Chao / Britton, Graham J / Chen-Liaw, Alice / Mitcham, Josephine / Bongers, Gerold / Gevers, Dirk / Clemente, Jose C / Colombel, Jean-Frederic / Grinspan, Ari / Faith, Jeremiah

    Nature microbiology

    2022  Band 7, Heft 5, Seite(n) 736

    Sprache Englisch
    Erscheinungsdatum 2022-04-06
    Erscheinungsland England
    Dokumenttyp Published Erratum
    ISSN 2058-5276
    ISSN (online) 2058-5276
    DOI 10.1038/s41564-022-01118-8
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  4. Artikel: Inhibition of exendin-4-induced steatosis by protein kinase A in cultured HepG2 human hepatoma cells

    Chen-Liaw, Alice Y / Gabrielle Hammel / George Gomez

    In vitro cellular & developmental biology. 2017 Sept., v. 53, no. 8

    2017  

    Abstract: Nonalcoholic fatty liver is characterized by the abnormal accumulation of triglycerides within hepatocytes, resulting in a steatotic liver. Glucagon-like peptide 1 and its analog exendin-4 can ameliorate certain aspects of this syndrome by inducing ... ...

    Abstract Nonalcoholic fatty liver is characterized by the abnormal accumulation of triglycerides within hepatocytes, resulting in a steatotic liver. Glucagon-like peptide 1 and its analog exendin-4 can ameliorate certain aspects of this syndrome by inducing weight loss and reducing hepatic triglyceride accumulation, but it is unclear whether these effects result from the effects of glucagon-like peptide 1 on the pancreas, or from direct action on the liver. This study investigated the direct action and putative cellular mechanism of exendin-4 on steatotic hepatocytes in culture. Steatosis was induced in cultured HepG2 human hepatoma cells by incubation in media supplemented with 2 mM each of linoleic acid and oleic acid. Steatotic hepatocytes were then pre-incubated in the protein kinase A inhibitor H89 for 30 min, then treated with exendin-4 over a period of 24 h. Cell viability and triglyceride content were characterized by a TUNEL assay and AdipoRed staining, respectively. Our results showed that steatotic cells maintained high levels of intracellular triglycerides (80%) compared to lean controls (25%). Exendin-4 treatment caused a significant reduction in intracellular triglyceride content after 12 h that persisted through 24 h, while protein kinase A inhibitors abolished the effects of exendin-4. The results demonstrate the exendin-4 induces a partial reduction in triglycerides in steatotic hepatocytes within 12 h via the GLP-1 receptor-mediated activation of protein kinase A. Thus, the reduction in hepatocyte triglyceride accumulation is likely driven primarily by downregulation of lipogenesis and upregulation of β-oxidation of free fatty acids.
    Schlagwörter beta oxidation ; cAMP-dependent protein kinase ; cell viability ; fatty liver ; free fatty acids ; glucagon-like peptide 1 ; hepatocytes ; hepatoma ; humans ; in vitro studies ; linoleic acid ; lipogenesis ; liver ; oleic acid ; pancreas ; staining ; triacylglycerols ; weight loss
    Sprache Englisch
    Erscheinungsverlauf 2017-09
    Umfang p. 721-727.
    Erscheinungsort Springer US
    Dokumenttyp Artikel
    ISSN 1071-2690
    DOI 10.1007/s11626-017-0181-y
    Datenquelle NAL Katalog (AGRICOLA)

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  5. Artikel ; Online: Precise quantification of bacterial strains after fecal microbiota transplantation delineates long-term engraftment and explains outcomes.

    Aggarwala, Varun / Mogno, Ilaria / Li, Zhihua / Yang, Chao / Britton, Graham J / Chen-Liaw, Alice / Mitcham, Josephine / Bongers, Gerold / Gevers, Dirk / Clemente, Jose C / Colombel, Jean-Frederic / Grinspan, Ari / Faith, Jeremiah

    Nature microbiology

    2021  Band 6, Heft 10, Seite(n) 1309–1318

    Abstract: Fecal microbiota transplantation (FMT) has been successfully applied to treat recurrent Clostridium difficile infection in humans, but a precise method to measure which bacterial strains stably engraft in recipients and evaluate their association with ... ...

    Abstract Fecal microbiota transplantation (FMT) has been successfully applied to treat recurrent Clostridium difficile infection in humans, but a precise method to measure which bacterial strains stably engraft in recipients and evaluate their association with clinical outcomes is lacking. We assembled a collection of >1,000 different bacterial strains that were cultured from the fecal samples of 22 FMT donors and recipients. Using our strain collection combined with metagenomic sequencing data from the same samples, we developed a statistical approach named Strainer for the detection and tracking of bacterial strains from metagenomic sequencing data. We applied Strainer to evaluate a cohort of 13 FMT longitudinal clinical interventions and detected stable engraftment of 71% of donor microbiota strains in recipients up to 5 years post-FMT. We found that 80% of recipient gut bacterial strains pre-FMT were eliminated by FMT and that post-FMT the strains present persisted up to 5 years later, together with environmentally acquired strains. Quantification of donor bacterial strain engraftment in recipients independently explained (precision 100%, recall 95%) the clinical outcomes (relapse or success) after initial and repeat FMT. We report a compendium of bacterial species and strains that consistently engraft in recipients over time that could be used in defined live biotherapeutic products as an alternative to FMT. Our analytical framework and Strainer can be applied to systematically evaluate either FMT or defined live bacterial therapeutic studies by quantification of strain engraftment in recipients.
    Mesh-Begriff(e) Algorithms ; Bacteria/classification ; Bacteria/genetics ; Bacteria/isolation & purification ; Benchmarking ; Clostridioides difficile/physiology ; Clostridium Infections/microbiology ; Clostridium Infections/therapy ; Fecal Microbiota Transplantation/methods ; Feces/microbiology ; Gastrointestinal Microbiome ; Humans ; Longitudinal Studies ; Metagenome/genetics ; Recurrence ; Tissue Donors ; Treatment Outcome
    Sprache Englisch
    Erscheinungsdatum 2021-09-27
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2058-5276
    ISSN (online) 2058-5276
    DOI 10.1038/s41564-021-00966-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Epigenomic regulation of human T-cell leukemia virus by chromatin-insulator CTCF.

    Cheng, Xiaogang / Joseph, Ancy / Castro, Victor / Chen-Liaw, Alice / Skidmore, Zachary / Ueno, Takaharu / Fujisawa, Jun-Ichi / Rauch, Daniel A / Challen, Grant A / Martinez, Michael P / Green, Patrick / Griffith, Malachi / Payton, Jacqueline E / Edwards, John R / Ratner, Lee

    PLoS pathogens

    2021  Band 17, Heft 5, Seite(n) e1009577

    Abstract: Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that causes an aggressive T-cell malignancy and a variety of inflammatory conditions. The integrated provirus includes a single binding site for the epigenomic insulator, CCCTC-binding protein ( ... ...

    Abstract Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that causes an aggressive T-cell malignancy and a variety of inflammatory conditions. The integrated provirus includes a single binding site for the epigenomic insulator, CCCTC-binding protein (CTCF), but its function remains unclear. In the current study, a mutant virus was examined that eliminates the CTCF-binding site. The mutation did not disrupt the kinetics and levels of virus gene expression, or establishment of or reactivation from latency. However, the mutation disrupted the epigenetic barrier function, resulting in enhanced DNA CpG methylation downstream of the CTCF binding site on both strands of the integrated provirus and H3K4Me3, H3K36Me3, and H3K27Me3 chromatin modifications both up- and downstream of the site. A majority of clonal cell lines infected with wild type HTLV-1 exhibited increased plus strand gene expression with CTCF knockdown, while expression in mutant HTLV-1 clonal lines was unaffected. These findings indicate that CTCF binding regulates HTLV-1 gene expression, DNA and histone methylation in an integration site dependent fashion.
    Mesh-Begriff(e) Binding Sites ; CCCTC-Binding Factor/genetics ; CCCTC-Binding Factor/metabolism ; Cell Line ; Chromatin/genetics ; DNA Methylation ; Epigenesis, Genetic ; Epigenomics ; Genome, Viral/genetics ; HTLV-I Infections/virology ; Human T-lymphotropic virus 1/genetics ; Human T-lymphotropic virus 1/physiology ; Humans ; Leukemia, T-Cell/virology ; Mutation ; Virus Integration ; Virus Latency/genetics
    Chemische Substanzen CCCTC-Binding Factor ; Chromatin
    Sprache Englisch
    Erscheinungsdatum 2021-05-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1009577
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Limited intestinal inflammation despite diarrhea, fecal viral RNA and SARS-CoV-2-specific IgA in patients with acute COVID-19.

    Britton, Graham J / Chen-Liaw, Alice / Cossarini, Francesca / Livanos, Alexandra E / Spindler, Matthew P / Plitt, Tamar / Eggers, Joseph / Mogno, Ilaria / Gonzalez-Reiche, Ana S / Siu, Sophia / Tankelevich, Michael / Grinspan, Lauren Tal / Dixon, Rebekah E / Jha, Divya / van de Guchte, Adriana / Khan, Zenab / Martinez-Delgado, Gustavo / Amanat, Fatima / Hoagland, Daisy A /
    tenOever, Benjamin R / Dubinsky, Marla C / Merad, Miriam / van Bakel, Harm / Krammer, Florian / Bongers, Gerold / Mehandru, Saurabh / Faith, Jeremiah J

    Scientific reports

    2021  Band 11, Heft 1, Seite(n) 13308

    Abstract: Gastrointestinal symptoms are common in COVID-19 patients but the nature of the gut immune response to SARS-CoV-2 remains poorly characterized, partly due to the difficulty of obtaining biopsy specimens from infected individuals. In lieu of tissue ... ...

    Abstract Gastrointestinal symptoms are common in COVID-19 patients but the nature of the gut immune response to SARS-CoV-2 remains poorly characterized, partly due to the difficulty of obtaining biopsy specimens from infected individuals. In lieu of tissue samples, we measured cytokines, inflammatory markers, viral RNA, microbiome composition, and antibody responses in stool samples from a cohort of 44 hospitalized COVID-19 patients. SARS-CoV-2 RNA was detected in stool of 41% of patients and more frequently in patients with diarrhea. Patients who survived had lower fecal viral RNA than those who died. Strains isolated from stool and nasopharynx of an individual were the same. Compared to uninfected controls, COVID-19 patients had higher fecal levels of IL-8 and lower levels of fecal IL-10. Stool IL-23 was higher in patients with more severe COVID-19 disease, and we found evidence of intestinal virus-specific IgA responses associated with more severe disease. We provide evidence for an ongoing humeral immune response to SARS-CoV-2 in the gastrointestinal tract, but little evidence of overt inflammation.
    Mesh-Begriff(e) Aged ; Biomarkers/metabolism ; COVID-19/epidemiology ; COVID-19/immunology ; Cohort Studies ; Cytokines/metabolism ; Feces/virology ; Female ; Gastrointestinal Microbiome ; Humans ; Immunoglobulin A/blood ; Immunoglobulin A/immunology ; Male ; Middle Aged ; Nasopharynx/virology ; New York City/epidemiology ; RNA, Viral/isolation & purification ; SARS-CoV-2/isolation & purification
    Chemische Substanzen Biomarkers ; Cytokines ; Immunoglobulin A ; RNA, Viral
    Sprache Englisch
    Erscheinungsdatum 2021-06-25
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-92740-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: Limited intestinal inflammation despite diarrhea, fecal viral RNA and SARS-CoV-2-specific IgA in patients with acute COVID-19.

    Britton, Graham J / Chen-Liaw, Alice / Cossarini, Francesca / Livanos, Alexandra E / Spindler, Matthew P / Plitt, Tamar / Eggers, Joseph / Mogno, Ilaria / Gonzalez-Reiche, Ana S / Siu, Sophia / Tankelevich, Michael / Grinspan, Lauren Tal / Dixon, Rebekah E / Jha, Divya / van de Guchte, Adriana / Khan, Zenab / Martinez-Delgado, Gustavo / Amanat, Fatima / Hoagland, Daisy A /
    tenOever, Benjamin R / Dubinsky, Marla C / Merad, Miriam / van Bakel, Harm / Krammer, Florian / Bongers, Gerold / Mehandru, Saurabh / Faith, Jeremiah J

    medRxiv : the preprint server for health sciences

    2020  

    Abstract: We sought to characterize the role of the gastrointestinal immune system in the pathogenesis of the inflammatory response associated with COVID-19. We measured cytokines, inflammatory markers, viral RNA, microbiome composition and antibody responses in ... ...

    Abstract We sought to characterize the role of the gastrointestinal immune system in the pathogenesis of the inflammatory response associated with COVID-19. We measured cytokines, inflammatory markers, viral RNA, microbiome composition and antibody responses in stool from a cohort of 44 hospitalized COVID-19 patients. SARS-CoV-2 RNA was detected in stool of 41% of patients and more frequently in patients with diarrhea. Patients who survived had lower fecal viral RNA than those who died. Strains isolated from stool and nasopharynx of an individual were the same. Compared to uninfected controls, COVID-19 patients had higher fecal levels of IL-8 and lower levels of fecal IL-10. Stool IL-23 was higher in patients with more severe COVID-19 disease, and we found evidence of intestinal virus-specific IgA responses associated with more severe disease. We provide evidence for an ongoing humeral immune response to SARS-CoV-2 in the gastrointestinal tract, but little evidence of overt inflammation.
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2020-12-09
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2020.09.03.20183947
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Intestinal Host Response to SARS-CoV-2 Infection and COVID-19 Outcomes in Patients With Gastrointestinal Symptoms.

    Livanos, Alexandra E / Jha, Divya / Cossarini, Francesca / Gonzalez-Reiche, Ana S / Tokuyama, Minami / Aydillo, Teresa / Parigi, Tommaso L / Ladinsky, Mark S / Ramos, Irene / Dunleavy, Katie / Lee, Brian / Dixon, Rebekah E / Chen, Steven T / Martinez-Delgado, Gustavo / Nagula, Satish / Bruce, Emily A / Ko, Huaibin M / Glicksberg, Benjamin S / Nadkarni, Girish /
    Pujadas, Elisabet / Reidy, Jason / Naymagon, Steven / Grinspan, Ari / Ahmad, Jawad / Tankelevich, Michael / Bram, Yaron / Gordon, Ronald / Sharma, Keshav / Houldsworth, Jane / Britton, Graham J / Chen-Liaw, Alice / Spindler, Matthew P / Plitt, Tamar / Wang, Pei / Cerutti, Andrea / Faith, Jeremiah J / Colombel, Jean-Frederic / Kenigsberg, Ephraim / Argmann, Carmen / Merad, Miriam / Gnjatic, Sacha / Harpaz, Noam / Danese, Silvio / Cordon-Cardo, Carlos / Rahman, Adeeb / Schwartz, Robert E / Kumta, Nikhil A / Aghemo, Alessio / Bjorkman, Pamela J / Petralia, Francesca / van Bakel, Harm / Garcia-Sastre, Adolfo / Mehandru, Saurabh

    Gastroenterology

    2021  Band 160, Heft 7, Seite(n) 2435–2450.e34

    Abstract: Background & aims: Given that gastrointestinal (GI) symptoms are a prominent extrapulmonary manifestation of COVID-19, we investigated intestinal infection with SARS-CoV-2, its effect on pathogenesis, and clinical significance.: Methods: Human ... ...

    Abstract Background & aims: Given that gastrointestinal (GI) symptoms are a prominent extrapulmonary manifestation of COVID-19, we investigated intestinal infection with SARS-CoV-2, its effect on pathogenesis, and clinical significance.
    Methods: Human intestinal biopsy tissues were obtained from patients with COVID-19 (n = 19) and uninfected control individuals (n = 10) for microscopic examination, cytometry by time of flight analyses, and RNA sequencing. Additionally, disease severity and mortality were examined in patients with and without GI symptoms in 2 large, independent cohorts of hospitalized patients in the United States (N = 634) and Europe (N = 287) using multivariate logistic regressions.
    Results: COVID-19 case patients and control individuals in the biopsy cohort were comparable for age, sex, rates of hospitalization, and relevant comorbid conditions. SARS-CoV-2 was detected in small intestinal epithelial cells by immunofluorescence staining or electron microscopy in 15 of 17 patients studied. High-dimensional analyses of GI tissues showed low levels of inflammation, including down-regulation of key inflammatory genes including IFNG, CXCL8, CXCL2, and IL1B and reduced frequencies of proinflammatory dendritic cells compared with control individuals. Consistent with these findings, we found a significant reduction in disease severity and mortality in patients presenting with GI symptoms that was independent of sex, age, and comorbid illnesses and despite similar nasopharyngeal SARS-CoV-2 viral loads. Furthermore, there was reduced levels of key inflammatory proteins in circulation in patients with GI symptoms.
    Conclusions: These data highlight the absence of a proinflammatory response in the GI tract despite detection of SARS-CoV-2. In parallel, reduced mortality in patients with COVID-19 presenting with GI symptoms was observed. A potential role of the GI tract in attenuating SARS-CoV-2-associated inflammation needs to be further examined.
    Mesh-Begriff(e) Aged ; Aged, 80 and over ; COVID-19/diagnosis ; COVID-19/immunology ; COVID-19/mortality ; COVID-19/virology ; Case-Control Studies ; Cells, Cultured ; Cytokines/blood ; Female ; Gastrointestinal Diseases/diagnosis ; Gastrointestinal Diseases/immunology ; Gastrointestinal Diseases/mortality ; Gastrointestinal Diseases/virology ; Host-Pathogen Interactions ; Humans ; Immunity, Mucosal ; Inflammation Mediators/blood ; Intestinal Mucosa/immunology ; Intestinal Mucosa/virology ; Italy ; Male ; Middle Aged ; New York City ; Prognosis ; Risk Assessment ; Risk Factors ; SARS-CoV-2/immunology ; SARS-CoV-2/pathogenicity ; Viral Load
    Chemische Substanzen Cytokines ; Inflammation Mediators
    Sprache Englisch
    Erscheinungsdatum 2021-03-04
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2021.02.056
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: SARS-CoV-2-specific IgA and limited inflammatory cytokines are present in the stool of select patients with acute COVID-19

    Britton, Graham J / Chen-Liaw, Alice / Cossarini, Francesca / Livanos, Alexandra E / Spindler, Matthew P / Plitt, Tamar / Eggers, Joseph / Mogno, Ilaria / Gonzalez-Reiche, Ana / Siu, Sophia / Tankelevich, Michael / Grinspan, Lauren / Dixon, Rebekah E / Jha, Divya / Martinez-Delgado, Gustavo / Amanat, Fatima / Hoagland, Daisy A / tenOever, Benjamin / Dubinsky, Marla C /
    Merad, Miriam / van Bakel, Harm / Krammer, Florian / Bongers, Gerold / Mehandru, Saurabh / Faith, Jeremiah J

    medRxiv

    Abstract: Background and aims: Immune dysregulation caused by SARS-CoV-2 infection is thought to play a pathogenic role in COVID-19. SARS-CoV-2 can infect a variety of host cells, including intestinal epithelial cells. We sought to characterize the role of the ... ...

    Abstract Background and aims: Immune dysregulation caused by SARS-CoV-2 infection is thought to play a pathogenic role in COVID-19. SARS-CoV-2 can infect a variety of host cells, including intestinal epithelial cells. We sought to characterize the role of the gastrointestinal immune system in the pathogenesis of the inflammatory response associated with COVID-19. Methods: We measured cytokines, inflammatory markers, viral RNA, microbiome composition and antibody responses in stool and serum samples from a prospectively enrolled cohort of 44 hospitalized COVID-19 patients. Results: SARS-CoV-2 RNA was detected in stool of 41% of patients and was found more frequently in patients with diarrhea than those without (16[44%] vs 5[19%], p=0.06). Patients who survived had lower median viral genome copies than those who did not (p=0.021). Compared to uninfected controls, COVID-19 patients had higher median fecal levels of IL-8 (166.5 vs 286.5 pg/mg; p=0.05) and lower levels of fecal IL-10 (678 vs 194 pg/mg; p<0.001) compared to uninfected controls. Stool IL-23 was higher in patients with more severe COVID-19 disease (223.8 vs 86.6 pg/mg; p=0.03) and we find evidence of intestinal virus-specific IgA responses, which was associated with more severe disease. Fecal cytokines and calprotectin levels were not correlated with gastrointestinal symptoms or with the level of virus detected. Conclusions: Although SARS-CoV-2 RNA was detectable in the stools of COVID-19 patients and select individuals had evidence for a specific mucosal IgA response, intestinal inflammation was limited, even in patients presenting with gastrointestinal symptoms.
    Schlagwörter covid19
    Sprache Englisch
    Erscheinungsdatum 2020-09-05
    Verlag Cold Spring Harbor Laboratory Press
    Dokumenttyp Artikel ; Online
    DOI 10.1101/2020.09.03.20183947
    Datenquelle COVID19

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