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  1. Article ; Online: Antiviral Responses of Tissue-resident CD49a

    Cooper, Grace E / Mayall, Jemma / Donovan, Chantal / Haw, Tatt J / Budden, Kurtis F / Hansbro, Nicole G / Blomme, Evy E / Maes, Tania / Kong, Chia Wei / Horvat, Jay C / Khakoo, Salim I / Wilkinson, Tom M A / Hansbro, Philip M / Staples, Karl J

    American journal of respiratory and critical care medicine

    2022  Volume 207, Issue 5, Page(s) 553–565

    Abstract: Rationale: ...

    Abstract Rationale:
    MeSH term(s) Humans ; Mice ; Animals ; Integrin alpha1/metabolism ; Influenza, Human/metabolism ; Integrin alpha2/metabolism ; Pulmonary Disease, Chronic Obstructive/genetics ; Killer Cells, Natural ; Lung/metabolism ; Lung Diseases/metabolism ; Antiviral Agents
    Chemical Substances Integrin alpha1 ; Integrin alpha2 ; Antiviral Agents
    Language English
    Publishing date 2022-09-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.202205-0848OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease.

    Blomme, Evy E / Provoost, Sharen / De Smet, Elise G / De Grove, Katrien C / Van Eeckhoutte, Hannelore P / De Volder, Joyceline / Hansbro, Philip M / Bonato, Matteo / Saetta, Marina / Wijnant, Sara Ra / Verhamme, Fien / Joos, Guy F / Bracke, Ken R / Brusselle, Guy G / Maes, Tania

    Clinical & translational immunology

    2021  Volume 10, Issue 6, Page(s) e1287

    Abstract: Objectives: Innate lymphoid cells (ILCs) secrete cytokines, such as IFN-γ, IL-13 and IL-17, which are linked to chronic obstructive pulmonary disease (COPD). Here, we investigated the role of pulmonary ILCs in COPD pathogenesis.: Methods: Lung ILC ... ...

    Abstract Objectives: Innate lymphoid cells (ILCs) secrete cytokines, such as IFN-γ, IL-13 and IL-17, which are linked to chronic obstructive pulmonary disease (COPD). Here, we investigated the role of pulmonary ILCs in COPD pathogenesis.
    Methods: Lung ILC subsets in COPD and control subjects were quantified using flow cytometry and associated with clinical parameters. Tissue localisation of ILC and T-cell subsets was determined by immunohistochemistry. Mice were exposed to air or cigarette smoke (CS) for 1, 4 or 24 weeks to investigate whether pulmonary ILC numbers and activation are altered and whether they contribute to CS-induced innate inflammatory responses.
    Results: Quantification of lung ILC subsets demonstrated that ILC1 frequency in the total ILC population was elevated in COPD and was associated with smoking and severity of respiratory symptoms (COPD Assessment Test [CAT] score). All three ILC subsets localised near lymphoid aggregates in COPD. In the COPD mouse model, CS exposure in C57BL/6J mice increased ILC numbers at all time points, with relative increases in ILC1 in bronchoalveolar lavage (BAL) fluid. Importantly, CS exposure induced increases in neutrophils, monocytes and dendritic cells that remained elevated in
    Conclusion: The ILC1 subset is increased in COPD patients and correlates with smoking and severity of respiratory symptoms. ILCs also increase upon CS exposure in C57BL/6J mice. In the absence of adaptive immunity, ILCs contribute to CS-induced pro-inflammatory mediator release, but are redundant in CS-induced innate inflammation.
    Language English
    Publishing date 2021-06-05
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2694482-0
    ISSN 2050-0068
    ISSN 2050-0068
    DOI 10.1002/cti2.1287
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Cytotoxic Essential Oils from Eryngium campestre and Eryngium amethystinum (Apiaceae) Growing in Central Italy.

    Cianfaglione, Kevin / Blomme, Evy E / Quassinti, Luana / Bramucci, Massimo / Lupidi, Giulio / Dall'Acqua, Stefano / Maggi, Filippo

    Chemistry & biodiversity

    2017  Volume 14, Issue 7

    Abstract: Eryngium campestre and E. amethystinum are thorny herbs belonging to the Apiaceae family and spontaneously growing in stony pastures and dry meadows, preferentially on calcareous substrates. In the Mediterranean countries, these plants have been used as ... ...

    Abstract Eryngium campestre and E. amethystinum are thorny herbs belonging to the Apiaceae family and spontaneously growing in stony pastures and dry meadows, preferentially on calcareous substrates. In the Mediterranean countries, these plants have been used as a food or traditional remedies to treat various ailments. In the present work, we have analyzed the chemical composition of the essential oils distilled from the aerial parts by GC-FID and GC/MS, and evaluated their cytotoxic effects on a panel of human cancer cells, namely A375 (human malignant melanoma), MDA-MB 231 cells (human breast adenocarcinoma), and HCT116 cells (human colon carcinoma), by the MTT assay. Furthermore, the Eryngium essential oils were evaluated for antioxidant and acetylcholinesterase (AChE) activities. The two essential oils were rich in sesquiterpene hydrocarbons, with germacrene D as the major compound, accompanied by allo-aromadendrene, β-elemene, spathulenol, and ledol. They turned out to be highly cytotoxic on the tumor cells, with IC
    MeSH term(s) Antineoplastic Agents, Phytogenic/isolation & purification ; Antineoplastic Agents, Phytogenic/pharmacology ; Antioxidants/isolation & purification ; Antioxidants/pharmacology ; Cell Line, Tumor ; Cholinesterase Inhibitors/isolation & purification ; Cholinesterase Inhibitors/pharmacology ; Cytotoxins/isolation & purification ; Eryngium/chemistry ; Humans ; Italy ; Oils, Volatile/chemistry ; Plant Components, Aerial/chemistry ; Sesquiterpenes
    Chemical Substances Antineoplastic Agents, Phytogenic ; Antioxidants ; Cholinesterase Inhibitors ; Cytotoxins ; Oils, Volatile ; Sesquiterpenes
    Language English
    Publishing date 2017-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2139001-0
    ISSN 1612-1880 ; 1612-1872
    ISSN (online) 1612-1880
    ISSN 1612-1872
    DOI 10.1002/cbdv.201700096
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Innate lymphoid cells in isocyanate-induced asthma: role of microRNA-155.

    Blomme, Evy E / Provoost, Sharen / Bazzan, Erica / Van Eeckhoutte, Hannelore P / Roffel, Mirjam P / Pollaris, Lore / Bontinck, Annelies / Bonato, Matteo / Vandenbroucke, Louise / Verhamme, Fien / Joos, Guy F / Cosio, Manuel G / Vanoirbeek, Jeroen A J / Brusselle, Guy G / Saetta, Marina / Maes, Tania

    The European respiratory journal

    2020  Volume 56, Issue 3

    Abstract: Background: Occupational asthma, induced by workplace exposures to low molecular weight agents such as toluene 2,4-diisocyanate (TDI), causes a significant burden to patients and society. Little is known about innate lymphoid cells (ILCs) in TDI-induced ...

    Abstract Background: Occupational asthma, induced by workplace exposures to low molecular weight agents such as toluene 2,4-diisocyanate (TDI), causes a significant burden to patients and society. Little is known about innate lymphoid cells (ILCs) in TDI-induced asthma. A critical regulator of ILC function is microRNA-155, a microRNA associated with asthma.
    Objective: To determine whether TDI exposure modifies the number of ILCs in the lung and whether microRNA-155 contributes to TDI-induced airway inflammation and hyperresponsiveness.
    Methods: C57BL/6 wild-type and microRNA-155 knockout mice were sensitised and challenged with TDI or vehicle. Intracellular cytokine expression in ILCs and T-cells was evaluated in bronchoalveolar lavage (BAL) fluid using flow cytometry. Peribronchial eosinophilia and goblet cells were evaluated on lung tissue, and airway hyperresponsiveness was measured using the forced oscillation technique. Putative type 2 ILCs (ILC2) were identified in bronchial biopsies of subjects with TDI-induced occupational asthma using immunohistochemistry. Human bronchial epithelial cells were exposed to TDI or vehicle.
    Results: TDI-exposed mice had higher numbers of airway goblet cells, BAL eosinophils, CD4
    Conclusion: TDI exposure is associated with increased numbers of ILCs. The proinflammatory microRNA-155 is crucial in a murine model of TDI asthma, suggesting its involvement in the pathogenesis of occupational asthma due to low molecular weight agents.
    MeSH term(s) Animals ; Bronchoalveolar Lavage Fluid ; Disease Models, Animal ; Humans ; Immunity, Innate ; Lymphocytes ; Mice ; Mice, Inbred C57BL ; MicroRNAs ; Toluene 2,4-Diisocyanate/toxicity
    Chemical Substances MIRN155 microRNA, human ; MicroRNAs ; Mirn155 microRNA, mouse ; Toluene 2,4-Diisocyanate (17X7AFZ1GH)
    Language English
    Publishing date 2020-09-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01289-2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: IL-33 signalling contributes to pollutant-induced allergic airway inflammation.

    De Grove, Katrien C / Provoost, Sharen / Braun, Harald / Blomme, Evy E / Teufelberger, Andrea R / Krysko, Olga / Beyaert, Rudi / Brusselle, Guy G / Joos, Guy F / Maes, Tania

    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology

    2018  Volume 48, Issue 12, Page(s) 1665–1675

    Abstract: Background: Clinical and experimental studies have identified a crucial role for IL-33 and its receptor ST2 in allergic asthma. Inhalation of traffic-related pollutants, such as diesel exhaust particles (DEP), facilitates the development of asthma and ... ...

    Abstract Background: Clinical and experimental studies have identified a crucial role for IL-33 and its receptor ST2 in allergic asthma. Inhalation of traffic-related pollutants, such as diesel exhaust particles (DEP), facilitates the development of asthma and can cause exacerbations of asthma. However, it is unknown whether IL-33/ST2 signalling contributes to the enhancing effects of air pollutants on allergic airway responses.
    Objective: We aim to investigate the functional role of IL-33/ST2 signalling in DEP-enhanced allergic airway responses, using an established murine model.
    Methods: C57BL/6J mice were exposed to saline, DEP alone, house dust mite (HDM) alone or combined DEP+HDM. To inhibit IL-33 signalling, recombinant soluble ST2 (r-sST2) was given prophylactically (ie, during the whole experimental protocol) or therapeutically (ie, at the end of the experimental protocol). Airway hyperresponsiveness and the airway inflammatory responses were assessed in bronchoalveolar lavage fluid (BALF) and lung.
    Results: Combined exposure to DEP+HDM increased IL-33 and ST2 expression in lung, elevated inflammatory responses and bronchial hyperresponsiveness compared to saline, sole DEP or sole HDM exposure. Prophylactic interference with the IL-33/ST2 signalling pathway impaired the DEP-enhanced allergic airway inflammation in the BALF, whereas effects on lung inflammation and airway hyperresponsiveness were minimal. Treatment with r-sST2 at the end of the experimental protocol did not modulate the DEP-enhanced allergic airway responses.
    Conclusion: Our data suggest that the IL-33/ST2 pathway contributes to the onset of DEP-enhanced allergic airway inflammation.
    MeSH term(s) Air Pollutants/adverse effects ; Allergens/immunology ; Animals ; Biomarkers ; Disease Models, Animal ; Female ; Interleukin-1 Receptor-Like 1 Protein/metabolism ; Interleukin-33/metabolism ; Leukocytes/immunology ; Leukocytes/metabolism ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Mice ; Particulate Matter/adverse effects ; Pyroglyphidae/immunology ; Recombinant Proteins/pharmacology ; Respiratory Hypersensitivity/drug therapy ; Respiratory Hypersensitivity/etiology ; Respiratory Hypersensitivity/metabolism ; Respiratory Hypersensitivity/pathology ; Respiratory Mucosa/immunology ; Respiratory Mucosa/metabolism ; Signal Transduction
    Chemical Substances Air Pollutants ; Allergens ; Biomarkers ; Interleukin-1 Receptor-Like 1 Protein ; Interleukin-33 ; Particulate Matter ; Recombinant Proteins
    Language English
    Publishing date 2018-09-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 645204-8
    ISSN 1365-2222 ; 0954-7894 ; 0960-2178
    ISSN (online) 1365-2222
    ISSN 0954-7894 ; 0960-2178
    DOI 10.1111/cea.13261
    Database MEDical Literature Analysis and Retrieval System OnLINE

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