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  1. Article ; Online: Experimental Model to Evaluate Resolution of Pneumonia.

    Villabona-Rueda, Andres / Wang, Daniel / D'Alessio, Franco R

    Journal of visualized experiments : JoVE

    2023  , Issue 192

    Abstract: Acute respiratory distress syndrome (ARDS) causes acute lung injury, characterized by rapid alveolar damage and severe hypoxemia. This, in turn, leads to high morbidity and mortality. Currently, there are no pre-clinical models that recapitulate the ... ...

    Abstract Acute respiratory distress syndrome (ARDS) causes acute lung injury, characterized by rapid alveolar damage and severe hypoxemia. This, in turn, leads to high morbidity and mortality. Currently, there are no pre-clinical models that recapitulate the complexity of human ARDS. However, infectious models of pneumonia (PNA) can replicate the main pathophysiological features of ARDS. Here, we describe a model of PNA induced by the intratracheal instillation of live Streptococcus pneumoniae and Klebsiella pneumoniae in C57BL6 mice. In order to evaluate and characterize the model, after inducing injury, we carried out serial measurements of body weight and bronchoalveolar lavage (BAL) for measuring markers of lung injury. Additionally, we harvested lungs for cell count and differentials, BAL protein quantification, cytospin, bacterial colony-forming unit counts, and histology. Lastly, high dimensional flow cytometry was performed. We propose this model as a tool to understand the immune landscape during the early and late resolution phases of lung injury.
    MeSH term(s) Animals ; Mice ; Humans ; Mice, Inbred C57BL ; Pneumonia ; Streptococcus pneumoniae ; Acute Lung Injury ; Dimercaprol ; Models, Theoretical
    Chemical Substances Dimercaprol (0CPP32S55X)
    Language English
    Publishing date 2023-02-17
    Publishing country United States
    Document type Journal Article ; Video-Audio Media ; Research Support, N.I.H., Extramural
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/63925
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Mouse Models of Acute Lung Injury and ARDS.

    D'Alessio, Franco R

    Methods in molecular biology (Clifton, N.J.)

    2018  Volume 1809, Page(s) 341–350

    Abstract: The acute respiratory distress syndrome (ARDS) is a devastating illness characterized by severe hypoxemia and diffuse alveolar damage. Direct lung infection is the leading cause of ARDS and can be modeled in mice using sterile models of inflammation or ... ...

    Abstract The acute respiratory distress syndrome (ARDS) is a devastating illness characterized by severe hypoxemia and diffuse alveolar damage. Direct lung infection is the leading cause of ARDS and can be modeled in mice using sterile models of inflammation or live pathogens. In this chapter, two mouse models for ARDS are defined. These include an infectious model of ARDS driven by direct administration of Streptococcus pneumoniae and a sterile inflammatory model mediated by intratracheal administration of lipopolysaccharide. Methods for growth and preparation of Streptococcus pneumoniae are provided as methods to assess lung inflammation and injury.
    MeSH term(s) Acute Lung Injury/etiology ; Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Animals ; Bronchoalveolar Lavage ; Disease Models, Animal ; Humans ; Lipopolysaccharides/adverse effects ; Mice ; Respiratory Distress Syndrome, Adult/etiology ; Respiratory Distress Syndrome, Adult/metabolism ; Respiratory Distress Syndrome, Adult/pathology
    Chemical Substances Lipopolysaccharides
    Language English
    Publishing date 2018-07-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-8570-8_22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Web Exclusive. Annals On Call - Regulatory T Cells: Treatment for COVID-19?

    Centor, Robert M / D'Alessio, Franco R

    Annals of internal medicine

    2020  Volume 173, Issue 5, Page(s) OC1

    Keywords covid19
    Language English
    Publishing date 2020-08-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 336-0
    ISSN 1539-3704 ; 0003-4819
    ISSN (online) 1539-3704
    ISSN 0003-4819
    DOI 10.7326/A19-0037
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    Ua VI Zs.178/2: Show issues Location:
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  4. Article ; Online: COVID-19 and myeloid cells: complex interplay correlates with lung severity.

    D'Alessio, Franco R / Heller, Nicola M

    The Journal of clinical investigation

    2020  Volume 130, Issue 12, Page(s) 6214–6217

    Abstract: COVID-19 spans a wide range of symptoms, sometimes with profound immune system involvement. How immune cell subsets change during the disease course and with disease severity needs further study. While myeloid cells have been shown to initiate and ... ...

    Abstract COVID-19 spans a wide range of symptoms, sometimes with profound immune system involvement. How immune cell subsets change during the disease course and with disease severity needs further study. While myeloid cells have been shown to initiate and maintain responses to pneumonia and lung inflammation, often playing a role in resolution, their involvement with COVID-19 remains unknown. In this issue of the JCI, Sánchez-Cerrillo and Landete et al. investigated DCs and monocytes from blood and bronchial secretions of patients with varying COVID-19 severity and with healthy controls. The authors conclude that circulating monocytes and DCs migrate from the blood into the inflamed lungs. While sampling differences in sex, collection timing, bacteria/fungal infection, and corticosteroid treatment limit interpretation, we believe that reprogramming monocyte or macrophages by targeting immunometabolism, epigenetics, or the cytokine milieu holds promise in resolving lung inflammation associated with COVID-19.
    MeSH term(s) COVID-19 ; Humans ; Lung ; Monocytes ; Pandemics ; SARS-CoV-2
    Keywords covid19
    Language English
    Publishing date 2020-10-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI143361
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  5. Article ; Online: The Transcriptional Signature in Alveolar Macrophages Dictates Acute Respiratory Distress Outcomes.

    Tejwani, Vickram / D'Alessio, Franco R

    American journal of respiratory and critical care medicine

    2019  Volume 200, Issue 6, Page(s) 656–657

    MeSH term(s) Bronchoalveolar Lavage Fluid ; Dyspnea ; Humans ; Macrophages, Alveolar ; Respiratory Distress Syndrome
    Language English
    Publishing date 2019-05-20
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.201905-0952ED
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  6. Article ; Online: Reparative T lymphocytes in organ injury.

    D'Alessio, Franco R / Kurzhagen, Johanna T / Rabb, Hamid

    The Journal of clinical investigation

    2019  Volume 129, Issue 7, Page(s) 2608–2618

    Abstract: Acute organ injuries such as acute cerebrovascular accidents, myocardial infarction, acute kidney injury, acute lung injury, and others are among the leading causes of death worldwide. Dysregulated or insufficient organ repair mechanisms limit ... ...

    Abstract Acute organ injuries such as acute cerebrovascular accidents, myocardial infarction, acute kidney injury, acute lung injury, and others are among the leading causes of death worldwide. Dysregulated or insufficient organ repair mechanisms limit restoration of homeostasis and contribute to chronic organ failure. Studies reveal that both humans and mice harness potent non-stem cells that are capable of directly or indirectly promoting tissue repair. Specific populations of T lymphocytes have emerged as important reparative cells with context-specific actions. These T cells can resolve inflammation and secrete reparative cytokines and growth factors as well as interact with other immune and stromal cells to promote the complex and active process of tissue repair. This Review focuses on the major populations of T lymphocytes known to mediate tissue repair, their reparative mechanisms, and the diseases in which they have been implicated. Elucidating and harnessing the mechanisms that promote the reparative functions of these T cells could greatly improve organ dysfunction after acute injury.
    MeSH term(s) Acute Lung Injury/immunology ; Acute Lung Injury/pathology ; Animals ; Cytokines/immunology ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Mice ; Myocardial Infarction/immunology ; Myocardial Infarction/pathology ; Regeneration/immunology ; Stroke/immunology ; Stroke/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
    Chemical Substances Cytokines
    Language English
    Publishing date 2019-07-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI124614
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Regulatory T Cells for Treating Patients With COVID-19 and Acute Respiratory Distress Syndrome: Two Case Reports.

    Gladstone, Douglas E / Kim, Bo Soo / Mooney, Kathy / Karaba, Andrew H / D'Alessio, Franco R

    Annals of internal medicine

    2020  Volume 173, Issue 10, Page(s) 852–853

    MeSH term(s) Aged ; Betacoronavirus ; COVID-19 ; Coronavirus Infections/therapy ; Humans ; Immunotherapy/methods ; Male ; Middle Aged ; Pandemics ; Pneumonia, Viral/therapy ; Respiratory Distress Syndrome/therapy ; Respiratory Distress Syndrome/virology ; SARS-CoV-2 ; T-Lymphocytes, Regulatory/physiology
    Keywords covid19
    Language English
    Publishing date 2020-07-06
    Publishing country United States
    Document type Case Reports ; Letter
    ZDB-ID 336-0
    ISSN 1539-3704 ; 0003-4819
    ISSN (online) 1539-3704
    ISSN 0003-4819
    DOI 10.7326/L20-0681
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  8. Article ; Online: Guide to assembling a successful K99/R00 application.

    Michaely, Peter / Bielinski, Suzette J / Campbell, Kenneth / D'Alessio, Franco / Dean, Delphine / Earley, Yumei Feng / Paine, Robert / Salama, Guy / Peter, Inga

    Journal of clinical and translational science

    2023  Volume 7, Issue 1, Page(s) e215

    Abstract: The National Institutes of Health's (NIH) K99/R00 Pathway to Independence Award offers promising postdoctoral researchers and clinician-scientists an opportunity to receive research support at both the mentored and the independent levels with the goal of ...

    Abstract The National Institutes of Health's (NIH) K99/R00 Pathway to Independence Award offers promising postdoctoral researchers and clinician-scientists an opportunity to receive research support at both the mentored and the independent levels with the goal of facilitating a timely transition to a tenure-track faculty position. This transitional program has been generally successful, with most K99/R00 awardees successfully securing R01-equivalent funding by the end of the R00 period. However, often highly promising proposals fail because of poor grantsmanship. This overview provides guidance from the perspective of long-standing members of the National Heart, Lung, and Blood Institute's Mentored Transition to Independence study section for the purpose of helping mentors and trainees regarding how best to assemble competitive K99/R00 applications.
    Language English
    Publishing date 2023-09-29
    Publishing country England
    Document type Journal Article
    ISSN 2059-8661
    ISSN (online) 2059-8661
    DOI 10.1017/cts.2023.639
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  9. Article ; Online: Estradiol resolves pneumonia via ERβ in regulatory T cells.

    Xiong, Ye / Zhong, Qiong / Palmer, Tsvi / Benner, Alison / Wang, Lan / Suresh, Karthik / Damico, Rachel / D'Alessio, Franco R

    JCI insight

    2021  Volume 6, Issue 3

    Abstract: Current treatments for pneumonia (PNA) are focused on the pathogens. Mortality from PNA-induced acute lung injury (PNA-ALI) remains high, underscoring the need for additional therapeutic targets. Clinical and experimental evidence exists for potential ... ...

    Abstract Current treatments for pneumonia (PNA) are focused on the pathogens. Mortality from PNA-induced acute lung injury (PNA-ALI) remains high, underscoring the need for additional therapeutic targets. Clinical and experimental evidence exists for potential sex differences in PNA survival, with males having higher mortality. In a model of severe pneumococcal PNA, when compared with male mice, age-matched female mice exhibited enhanced resolution characterized by decreased alveolar and lung inflammation and increased numbers of Tregs. Recognizing the critical role of Tregs in lung injury resolution, we evaluated whether improved outcomes in female mice were due to estradiol (E2) effects on Treg biology. E2 promoted a Treg-suppressive phenotype in vitro and resolution of PNA in vivo. Systemic rescue administration of E2 promoted resolution of PNA in male mice independent of lung bacterial clearance. E2 augmented Treg expression of Foxp3, CD25, and GATA3, an effect that required ERβ, and not ERα, signaling. Importantly, the in vivo therapeutic effects of E2 were lost in Treg-depleted mice (Foxp3DTR mice). Adoptive transfer of ex vivo E2-treated Tregs rescued Streptococcus pneumoniae-induce PNA-ALI, a salutary effect that required Treg ERβ expression. E2/ERβ was required for Tregs to control macrophage proinflammatory responses. Our findings support the therapeutic role for E2 in promoting resolution of lung inflammation after PNA via ERβ Tregs.
    MeSH term(s) Acute Lung Injury/drug therapy ; Acute Lung Injury/immunology ; Acute Lung Injury/metabolism ; Adoptive Transfer ; Animals ; Disease Models, Animal ; Estradiol/metabolism ; Estradiol/pharmacology ; Estrogen Receptor beta/deficiency ; Estrogen Receptor beta/genetics ; Estrogen Receptor beta/metabolism ; Female ; Lung/drug effects ; Lung/immunology ; Lung/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Pneumonia, Pneumococcal/drug therapy ; Pneumonia, Pneumococcal/immunology ; Pneumonia, Pneumococcal/metabolism ; Pulmonary Alveoli/drug effects ; Pulmonary Alveoli/immunology ; Pulmonary Alveoli/pathology ; Sex Factors ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
    Chemical Substances Estrogen Receptor beta ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2021-02-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.133251
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  10. Article ; Online: Histone/protein deacetylase 3 dictates critical aspects of regulatory T cell development and function.

    Singer, Benjamin D / D'Alessio, Franco R

    Cellular & molecular immunology

    2015  Volume 13, Issue 4, Page(s) 415–417

    MeSH term(s) Histone Deacetylase Inhibitors ; Histones ; T-Lymphocytes, Regulatory
    Chemical Substances Histone Deacetylase Inhibitors ; Histones
    Language English
    Publishing date 2015-06-15
    Publishing country China
    Document type Journal Article ; Comment
    ZDB-ID 2435097-7
    ISSN 2042-0226 ; 1672-7681
    ISSN (online) 2042-0226
    ISSN 1672-7681
    DOI 10.1038/cmi.2015.51
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