LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 6 of total 6

Search options

  1. Article ; Online: Sex and gender in asthma.

    Chowdhury, Nowrin U / Guntur, Vamsi P / Newcomb, Dawn C / Wechsler, Michael E

    European respiratory review : an official journal of the European Respiratory Society

    2021  Volume 30, Issue 162

    Abstract: Asthma is a heterogenous disease, and its prevalence and severity are different in ... ...

    Abstract Asthma is a heterogenous disease, and its prevalence and severity are different in males
    MeSH term(s) Adult ; Asthma/diagnosis ; Asthma/drug therapy ; Asthma/epidemiology ; COVID-19 ; Child ; Female ; Gonadal Steroid Hormones ; Humans ; Male ; Pregnancy ; Prevalence ; SARS-CoV-2 ; Sex Factors
    Chemical Substances Gonadal Steroid Hormones
    Language English
    Publishing date 2021-11-17
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1077620-5
    ISSN 1600-0617 ; 0905-9180
    ISSN (online) 1600-0617
    ISSN 0905-9180
    DOI 10.1183/16000617.0067-2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 3265: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: MicroRNA expression associated with low-grade cervical intraepithelial neoplasia outcomes.

    Winters, Ashley N / Berry, Alex K / Dewenter, Tracy A / Chowdhury, Nowrin U / Wright, Kelly L / Cameron, Jennifer E

    Journal of cancer research and clinical oncology

    2023  Volume 149, Issue 13, Page(s) 11969–11978

    Abstract: Purpose: Only a fraction of low-grade cervical intraepithelial neoplasia (CIN) progresses to high-grade CIN; however, the biological processes that differentiate progressive CIN from CIN that resolves naturally are poorly understood. MicroRNAs (miRNAs) ... ...

    Abstract Purpose: Only a fraction of low-grade cervical intraepithelial neoplasia (CIN) progresses to high-grade CIN; however, the biological processes that differentiate progressive CIN from CIN that resolves naturally are poorly understood. MicroRNAs (miRNAs) are important epigenetic regulators of gene expression and thus, miRNA expression profiling can reveal the dysregulated biology underlying disease processes. The purpose of this case-control study was to reveal miRNA expression patterns and predict the underlying biological pathways that are associated with clinical outcomes of low-grade CIN.
    Methods: Women with low-grade CIN diagnosis and definitive clinical outcomes (n = 51) were identified retrospectively using electronic clinical records. Comprehensive miRNA expression profiling was performed on the low-grade CIN diagnostic cervical biopsies retrieved from pathology archives. Differential miRNA expression was analyzed by comparing women with CIN that progressed to women with CIN that resolved naturally.
    Results: Differential expression of 29 miRNAs was observed in low-grade CIN that progressed to high-grade compared to low-grade CIN that resolved. Of these, 24 were significantly downregulated in progressive CIN, including miR-638, miR-3196, miR-4488, and miR-4508, while 5 miRNAs, including miR-1206a, were significantly upregulated. Computational gene ontology analysis based on the discovered miRNAs and their putative mRNA targets revealed biological processes associated with oncogenic phenotypes.
    Conclusion: Distinct miRNA expression profiles are associated with clinical outcomes of low-grade CIN. The functional effects of the differentially expressed miRNAs may be biological determinants of CIN progression or resolution.
    MeSH term(s) Humans ; Female ; Uterine Cervical Neoplasms/genetics ; Uterine Cervical Neoplasms/pathology ; Case-Control Studies ; Retrospective Studies ; Gene Expression Regulation, Neoplastic ; Uterine Cervical Dysplasia/pathology ; MicroRNAs/genetics ; MicroRNAs/metabolism
    Chemical Substances MicroRNAs ; MIRN638 microRNA, human
    Language English
    Publishing date 2023-07-08
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 134792-5
    ISSN 1432-1335 ; 0171-5216 ; 0084-5353 ; 0943-9382
    ISSN (online) 1432-1335
    ISSN 0171-5216 ; 0084-5353 ; 0943-9382
    DOI 10.1007/s00432-023-05023-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.10: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Androgen receptor signaling promotes Treg suppressive function during allergic airway inflammation.

    Gandhi, Vivek D / Cephus, Jacqueline-Yvonne / Norlander, Allison E / Chowdhury, Nowrin U / Zhang, Jian / Ceneviva, Zachary J / Tannous, Elie / Polosukhin, Vasiliy V / Putz, Nathan D / Wickersham, Nancy / Singh, Amrit / Ware, Lorraine B / Bastarache, Julie A / Shaver, Ciara M / Chu, Hong Wei / Peebles, R Stokes / Newcomb, Dawn C

    The Journal of clinical investigation

    2022  Volume 132, Issue 4

    Abstract: Women have higher prevalence of asthma compared with men. In asthma, allergic airway inflammation is initiated by IL-33 signaling through ST2, leading to increased IL-4, IL-5, and IL-13 production and eosinophil infiltration. Foxp3+ Tregs suppress and ... ...

    Abstract Women have higher prevalence of asthma compared with men. In asthma, allergic airway inflammation is initiated by IL-33 signaling through ST2, leading to increased IL-4, IL-5, and IL-13 production and eosinophil infiltration. Foxp3+ Tregs suppress and ST2+ Tregs promote allergic airway inflammation. Clinical studies showed that the androgen dehydroepiandrosterone (DHEA) reduced asthma symptoms in patients, and mouse studies showed that androgen receptor (AR) signaling decreased allergic airway inflammation. Yet the impact of AR signaling on lung Tregs remains unclear. Using AR-deficient and Foxp3 fate-mapping mice, we determined that AR signaling increased Treg suppression during Alternaria extract (Alt Ext; allergen) challenge by stabilizing Foxp3+ Tregs and limiting the number of ST2+ ex-Tregs and IL-13+ Th2 cells and ex-Tregs. AR signaling also decreased Alt Ext-induced ST2+ Tregs in mice by limiting expression of Gata2, a transcription factor for ST2, and by decreasing Alt Ext-induced IL-33 production from murine airway epithelial cells. We confirmed our findings in human cells where 5α-dihydrotestosterone (DHT), an androgen, decreased IL-33-induced ST2 expression in lung Tregs and decreased Alt Ext-induced IL-33 secretion in human bronchial epithelial cells. Our findings showed that AR signaling stabilized Treg suppressive function, providing a mechanism for the sex difference in asthma.
    MeSH term(s) Animals ; Asthma/genetics ; Asthma/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Receptors, Androgen/genetics ; Receptors, Androgen/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances Receptors, Androgen
    Language English
    Publishing date 2022-01-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI153397
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: Prostaglandin I2 signaling licenses Treg suppressive function and prevents pathogenic reprogramming.

    Norlander, Allison E / Bloodworth, Melissa H / Toki, Shinji / Zhang, Jian / Zhou, Weisong / Boyd, Kelli / Polosukhin, Vasiliy V / Cephus, Jacqueline-Yvonne / Ceneviva, Zachary J / Gandhi, Vivek D / Chowdhury, Nowrin U / Charbonnier, Louis-Marie / Rogers, Lisa M / Wang, Janey / Aronoff, David M / Bastarache, Lisa / Newcomb, Dawn C / Chatila, Talal A / Peebles, R Stokes

    The Journal of clinical investigation

    2021  Volume 131, Issue 7

    Abstract: Tregs restrain both the innate and adaptive immune systems to maintain homeostasis. Allergic airway inflammation, characterized by a Th2 response that results from a breakdown of tolerance to innocuous environmental antigens, is negatively regulated by ... ...

    Abstract Tregs restrain both the innate and adaptive immune systems to maintain homeostasis. Allergic airway inflammation, characterized by a Th2 response that results from a breakdown of tolerance to innocuous environmental antigens, is negatively regulated by Tregs. We previously reported that prostaglandin I2 (PGI2) promoted immune tolerance in models of allergic inflammation; however, the effect of PGI2 on Treg function was not investigated. Tregs from mice deficient in the PGI2 receptor IP (IP KO) had impaired suppressive capabilities during allergic airway inflammatory responses compared with mice in which PGI2 signaling was intact. IP KO Tregs had significantly enhanced expression of immunoglobulin-like transcript 3 (ILT3) compared with WT Tregs, which may contribute to the impairment of the IP KO Treg's ability to suppress Th2 responses. Using fate-mapping mice, we reported that PGI2 signaling prevents Treg reprogramming toward a pathogenic phenotype. PGI2 analogs promoted the differentiation of naive T cells to Tregs in both mice and humans via repression of β-catenin signaling. Finally, a missense variant in IP in humans was strongly associated with chronic obstructive asthma. Together, these data support that PGI2 signaling licenses Treg suppressive function and that PGI2 is a therapeutic target for enhancing Treg function.
    MeSH term(s) Animals ; Asthma/genetics ; Asthma/immunology ; Asthma/pathology ; Cellular Reprogramming/genetics ; Cellular Reprogramming/immunology ; Chronic Disease ; Epoprostenol/genetics ; Epoprostenol/immunology ; Humans ; Immune Tolerance ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Receptors, Epoprostenol/genetics ; Receptors, Epoprostenol/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/pathology
    Chemical Substances Receptors, Epoprostenol ; Epoprostenol (DCR9Z582X0)
    Language English
    Publishing date 2021-02-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI140690
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Targeting In Vivo Metabolic Vulnerabilities of Th2 and Th17 Cells Reduces Airway Inflammation.

    Healey, Diana C Contreras / Cephus, Jacqueline Y / Barone, Sierra M / Chowdhury, Nowrin U / Dahunsi, Debolanle O / Madden, Matthew Z / Ye, Xiang / Yu, Xuemei / Olszewski, Kellen / Young, Kirsten / Gerriets, Valerie A / Siska, Peter J / Dworski, Ryszard / Hemler, Jonathan / Locasale, Jason W / Poyurovsky, Masha V / Peebles, R Stokes / Irish, Jonathan M / Newcomb, Dawn C /
    Rathmell, Jeffrey C

    Journal of immunology (Baltimore, Md. : 1950)

    2021  Volume 206, Issue 6, Page(s) 1127–1139

    Abstract: T effector cells promote inflammation in asthmatic patients, and both Th2 and Th17 CD4 T cells have been implicated in severe forms of the disease. The metabolic phenotypes and dependencies of these cells, however, remain poorly understood in the ... ...

    Abstract T effector cells promote inflammation in asthmatic patients, and both Th2 and Th17 CD4 T cells have been implicated in severe forms of the disease. The metabolic phenotypes and dependencies of these cells, however, remain poorly understood in the regulation of airway inflammation. In this study, we show the bronchoalveolar lavage fluid of asthmatic patients had markers of elevated glucose and glutamine metabolism. Further, peripheral blood T cells of asthmatics had broadly elevated expression of metabolic proteins when analyzed by mass cytometry compared with healthy controls. Therefore, we hypothesized that glucose and glutamine metabolism promote allergic airway inflammation. We tested this hypothesis in two murine models of airway inflammation. T cells from lungs of mice sensitized with
    MeSH term(s) Adult ; Alternaria/immunology ; Animals ; Asthma/blood ; Asthma/drug therapy ; Asthma/immunology ; Biomarkers/analysis ; Biomarkers/metabolism ; Blood Glucose/metabolism ; Bronchoalveolar Lavage Fluid/immunology ; Case-Control Studies ; Cells, Cultured ; Dexamethasone/pharmacology ; Dexamethasone/therapeutic use ; Disease Models, Animal ; Drug Synergism ; Female ; Glucose Transporter Type 1/antagonists & inhibitors ; Glucose Transporter Type 1/metabolism ; Glutaminase/antagonists & inhibitors ; Glutaminase/metabolism ; Glutamine/metabolism ; Healthy Volunteers ; Humans ; Immunosuppressive Agents/pharmacology ; Immunosuppressive Agents/therapeutic use ; Lung/cytology ; Lung/drug effects ; Lung/immunology ; Male ; Mice ; Middle Aged ; Primary Cell Culture ; Pyroglyphidae/immunology ; Th17 Cells/drug effects ; Th17 Cells/immunology ; Th17 Cells/metabolism ; Th2 Cells/drug effects ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Young Adult
    Chemical Substances Biomarkers ; Blood Glucose ; Glucose Transporter Type 1 ; Immunosuppressive Agents ; Slc2a1 protein, mouse ; Glutamine (0RH81L854J) ; Dexamethasone (7S5I7G3JQL) ; Glutaminase (EC 3.5.1.2)
    Language English
    Publishing date 2021-02-08
    Publishing country United States
    Document type Journal Article ; Observational Study ; Research Support, N.I.H., Extramural
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.2001029
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.37: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 28: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: MTHFD2 is a metabolic checkpoint controlling effector and regulatory T cell fate and function.

    Sugiura, Ayaka / Andrejeva, Gabriela / Voss, Kelsey / Heintzman, Darren R / Xu, Xincheng / Madden, Matthew Z / Ye, Xiang / Beier, Katherine L / Chowdhury, Nowrin U / Wolf, Melissa M / Young, Arissa C / Greenwood, Dalton L / Sewell, Allison E / Shahi, Shailesh K / Freedman, Samantha N / Cameron, Alanna M / Foerch, Patrik / Bourne, Tim / Garcia-Canaveras, Juan C /
    Karijolich, John / Newcomb, Dawn C / Mangalam, Ashutosh K / Rabinowitz, Joshua D / Rathmell, Jeffrey C

    Immunity

    2021  Volume 55, Issue 1, Page(s) 65–81.e9

    Abstract: Antigenic stimulation promotes T cell metabolic reprogramming to meet increased biosynthetic, bioenergetic, and signaling demands. We show that the one-carbon (1C) metabolism enzyme methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) regulates de novo ... ...

    Abstract Antigenic stimulation promotes T cell metabolic reprogramming to meet increased biosynthetic, bioenergetic, and signaling demands. We show that the one-carbon (1C) metabolism enzyme methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) regulates de novo purine synthesis and signaling in activated T cells to promote proliferation and inflammatory cytokine production. In pathogenic T helper-17 (Th17) cells, MTHFD2 prevented aberrant upregulation of the transcription factor FoxP3 along with inappropriate gain of suppressive capacity. MTHFD2 deficiency also promoted regulatory T (Treg) cell differentiation. Mechanistically, MTHFD2 inhibition led to depletion of purine pools, accumulation of purine biosynthetic intermediates, and decreased nutrient sensor mTORC1 signaling. MTHFD2 was also critical to regulate DNA and histone methylation in Th17 cells. Importantly, MTHFD2 deficiency reduced disease severity in multiple in vivo inflammatory disease models. MTHFD2 is thus a metabolic checkpoint to integrate purine metabolism with pathogenic effector cell signaling and is a potential therapeutic target within 1C metabolism pathways.
    MeSH term(s) Animals ; Cell Differentiation ; Cytokines/metabolism ; DNA Methylation ; Disease Models, Animal ; Humans ; Inflammation/immunology ; Inflammation Mediators/metabolism ; Lymphocyte Activation ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Methylenetetrahydrofolate Dehydrogenase (NADP)/genetics ; Methylenetetrahydrofolate Dehydrogenase (NADP)/metabolism ; Mice ; Mice, Transgenic ; Mutation/genetics ; Purines/biosynthesis ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology
    Chemical Substances Cytokines ; Inflammation Mediators ; Purines ; Methylenetetrahydrofolate Dehydrogenase (NADP) (EC 1.5.1.5) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2021-11-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2021.10.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 4227: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 69: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top