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  1. Article ; Online: HIF2 keeps paces in tight hypoxic spaces.

    Colgan, Sean P

    Blood

    2021  Volume 137, Issue 24, Page(s) 3323–3324

    MeSH term(s) Basic Helix-Loop-Helix Transcription Factors/genetics ; Humans ; Hypoxia
    Chemical Substances Basic Helix-Loop-Helix Transcription Factors
    Language English
    Publishing date 2021-06-17
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2021011009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The hypoxic tissue microenvironment as a driver of mucosal inflammatory resolution.

    Cartwright, Ian M / Colgan, Sean P

    Frontiers in immunology

    2023  Volume 14, Page(s) 1124774

    Abstract: On the backdrop of all acute inflammatory processes lies the activation of the resolution response. Recent years have witnessed an emerging interest in defining molecular factors that influence the resolution of inflammation. A keystone feature of the ... ...

    Abstract On the backdrop of all acute inflammatory processes lies the activation of the resolution response. Recent years have witnessed an emerging interest in defining molecular factors that influence the resolution of inflammation. A keystone feature of the mucosal inflammatory microenvironment is hypoxia. The gastrointestinal tract, particularly the colon, exists in a state of physiological hypoxia and during active inflammation, this hypoxic state is enhanced as a result of infiltrating leukocyte oxygen consumption and the activation of oxygen consuming enzymes. Most evidence suggests that mucosal hypoxia promotes the active resolution of inflammation through a variety of mechanisms, including extracellular acidification, purine biosynthesis/salvage, the generation of specialized pro-resolving lipid mediators (ie. resolvins) and altered chemokine/cytokine expression. It is now appreciated that infiltrating innate immune cells (neutrophils, eosinophils, macrophages) have an important role in molding the tissue microenvironment to program an active resolution response. Structural or functional dysregulation of this inflammatory microenvironment can result in the loss of tissue homeostasis and ultimately progression toward chronicity. In this review, we will discuss how inflammatory hypoxia drives mucosal inflammatory resolution and its impact on other microenvironmental factors that influence resolution.
    MeSH term(s) Humans ; Inflammation ; Hypoxia ; Mucous Membrane/metabolism ; Neutrophils ; Mucositis
    Language English
    Publishing date 2023-01-18
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1124774
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  3. Article ; Online: Resolvins resolve to heal mucosal wounds.

    Colgan, Sean P

    Proceedings of the National Academy of Sciences of the United States of America

    2020  Volume 117, Issue 20, Page(s) 10621–10622

    MeSH term(s) Eicosapentaenoic Acid/analogs & derivatives ; Intestines ; Mucous Membrane ; Wound Healing
    Chemical Substances Eicosapentaenoic Acid (AAN7QOV9EA) ; 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid (GND3JH08JA)
    Language English
    Publishing date 2020-05-05
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2005652117
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
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  4. Book: Cell cell interactions

    Colgan, Sean P.

    methods and protocols

    (Methods in molecular biology ; 341)

    2006  

    Title variant Cell-cell interactions
    Author's details ed. by Sean P. Colgan
    Series title Methods in molecular biology ; 341
    Collection
    Keywords Cell Communication / physiology ; Tight Junctions / physiology ; Endothelial Cells / physiology ; Epithelial Cells / physiology
    Language English
    Size XIII, 386 S., [2] Bl. : Ill., graph. Darst.
    Publisher Humana Press
    Publishing place Totowa, NJ
    Publishing country United States
    Document type Book
    Note Includes bibliographical references and index
    HBZ-ID HT014698827
    ISBN 978-1-58829-523-1 ; 1-58829-523-0
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2006 A 3413 order for loan Magazin

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  5. Article ; Online: Allopurinol Disrupts Purine Metabolism to Increase Damage in Experimental Colitis.

    Worledge, Corey S / Kostelecky, Rachael E / Zhou, Liheng / Bhagavatula, Geetha / Colgan, Sean P / Lee, J Scott

    Cells

    2024  Volume 13, Issue 5

    Abstract: Inflammatory bowel disease (IBD) is marked by a state of chronic energy deficiency that limits gut tissue wound healing. This energy shortfall is partially due to microbiota dysbiosis, resulting in the loss of microbiota-derived metabolites, which the ... ...

    Abstract Inflammatory bowel disease (IBD) is marked by a state of chronic energy deficiency that limits gut tissue wound healing. This energy shortfall is partially due to microbiota dysbiosis, resulting in the loss of microbiota-derived metabolites, which the epithelium relies on for energy procurement. The role of microbiota-sourced purines, such as hypoxanthine, as substrates salvaged by the colonic epithelium for nucleotide biogenesis and energy balance, has recently been appreciated for homeostasis and wound healing. Allopurinol, a synthetic hypoxanthine isomer commonly prescribed to treat excess uric acid in the blood, inhibits the degradation of hypoxanthine by xanthine oxidase, but also inhibits purine salvage. Although the use of allopurinol is common, studies regarding how allopurinol influences the gastrointestinal tract during colitis are largely nonexistent. In this work, a series of
    MeSH term(s) Humans ; Mice ; Animals ; Allopurinol ; Purines/metabolism ; Hypoxanthine/metabolism ; Colitis/drug therapy ; Inflammatory Bowel Diseases/drug therapy
    Chemical Substances Allopurinol (63CZ7GJN5I) ; Purines ; Hypoxanthine (2TN51YD919)
    Language English
    Publishing date 2024-02-21
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells13050373
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  6. Article ; Online: Lung neutrophils on a paleo diet: lean, mean inflammatory machines.

    Cartwright, Ian M / Colgan, Sean P

    The Journal of clinical investigation

    2021  Volume 131, Issue 10

    Abstract: Sites of acute inflammation become austere environments for the procurement of energy. The combination of oxygen depletion (hypoxia) and decreased glucose availability requires surprising metabolic adaptability. In this issue of the JCI, Watts et al. ... ...

    Abstract Sites of acute inflammation become austere environments for the procurement of energy. The combination of oxygen depletion (hypoxia) and decreased glucose availability requires surprising metabolic adaptability. In this issue of the JCI, Watts et al. examined the metabolic adaptability of murine neutrophils to the setting of acute pulmonary inflammation elicited by exposure to nebulized endotoxin. While neutrophils are generally considered a primarily glycolytic cell type, Watts et al. used a combination of labeled amino acids and high-resolution proteomics to reveal that the harsh environment of the inflammatory lesion drives neutrophils toward de novo protein synthesis and extracellular protein scavenging as a primary fuel. This study provides compelling evidence that tissue neutrophils scavenge extracellular proteins to fuel carbon metabolism, which aids in de novo protein synthesis and the promotion of an inflammatory phenotype. These observations reveal the surprisingly creative extent to which cells and tissues might adapt to energy-deficient inflammatory environments.
    MeSH term(s) Animals ; Diet, Paleolithic ; Endotoxins ; Glycolysis ; Lung ; Mice ; Neutrophils
    Chemical Substances Endotoxins
    Language English
    Publishing date 2021-05-17
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI149495
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    Ua VI Zs.184: Show issues Location:
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  7. Article: Metabolic Host-Microbiota Interactions in Autophagy and the Pathogenesis of Inflammatory Bowel Disease (IBD).

    Dowdell, Alexander S / Colgan, Sean P

    Pharmaceuticals (Basel, Switzerland)

    2021  Volume 14, Issue 8

    Abstract: Inflammatory bowel disease (IBD) is a family of conditions characterized by chronic, relapsing inflammation of the gastrointestinal tract. IBD afflicts over 3 million adults in the United States and shows increasing prevalence in the Westernized world. ... ...

    Abstract Inflammatory bowel disease (IBD) is a family of conditions characterized by chronic, relapsing inflammation of the gastrointestinal tract. IBD afflicts over 3 million adults in the United States and shows increasing prevalence in the Westernized world. Current IBD treatments center on modulation of the damaging inflammatory response and carry risks such as immunosuppression, while the development of more effective treatments is hampered by our poor understanding of the molecular mechanisms of IBD pathogenesis. Previous genome-wide association studies (GWAS) have demonstrated that gene variants linked to the cellular response to microorganisms are most strongly associated with an increased risk of IBD. These studies are supported by mechanistic work demonstrating that IBD-associated polymorphisms compromise the intestine's anti-microbial defense. In this review, we summarize the current knowledge regarding IBD as a disease of defects in host-microbe interactions and discuss potential avenues for targeting this mechanism for future therapeutic development.
    Language English
    Publishing date 2021-07-22
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph14080708
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  8. Article ; Online: In vitro Monitoring of Extracellular pH in Real-Time.

    Cartwright, Ian M / Colgan, Sean P

    Journal of visualized experiments : JoVE

    2021  , Issue 172

    Abstract: Early accumulation of neutrophils (PMN) is a hallmark of acute intestinal inflammation. This acute inflammation is either resolved or progresses to chronic inflammation. Without efficient PMN clearance at sites of infiltration, PMN can accumulate and ... ...

    Abstract Early accumulation of neutrophils (PMN) is a hallmark of acute intestinal inflammation. This acute inflammation is either resolved or progresses to chronic inflammation. Without efficient PMN clearance at sites of infiltration, PMN can accumulate and contribute to chronic inflammatory conditions, including the intestinal diseases ulcerative colitis (UC) and Crohn's Disease (CD). The pH in the distal colon in individuals with active UC can range between a pH of 5 and 6, whereas healthy individuals maintain colonic pH in the range of 6.8-7.4. Extracellular pH has been shown to influence both intestinal epithelial cells and the infiltrating immune cells. More specifically, extracellular acidosis significantly impacts PMN. At pH below 6.5, there are increases in the production of H2O2, inhibition of apoptosis, and increases in the functional lifespan of PMN. Given the significant presence of PMN and extracellular acidification at sites of inflammation, we developed a novel model that allows for the monitoring of extracellular pH during PMN transepithelial migration in real time. Here, we describe this model and how it can be utilized to measure both the apical and basal pH during PMN trafficking. This model can be utilized to monitor extracellular pH under a wide range of conditions; including, hypoxia, PMN transepithelial migration, and for extended periods of time.
    MeSH term(s) Colon ; Humans ; Hydrogen Peroxide ; Hydrogen-Ion Concentration ; Intestinal Mucosa ; Neutrophils
    Chemical Substances Hydrogen Peroxide (BBX060AN9V)
    Language English
    Publishing date 2021-06-03
    Publishing country United States
    Document type Journal Article ; Video-Audio Media
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/62169
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  9. Article ; Online: Targeting hypoxia in inflammatory bowel disease.

    Colgan, Sean P

    Journal of investigative medicine : the official publication of the American Federation for Clinical Research

    2016  Volume 64, Issue 2, Page(s) 364–368

    Abstract: In this review, I summarize some of the recent insight into pharmacological targeting of hypoxia in disease models. Studies from cultured cell systems, animal models, and translation to human patients have revealed that posttranslational modifications of ...

    Abstract In this review, I summarize some of the recent insight into pharmacological targeting of hypoxia in disease models. Studies from cultured cell systems, animal models, and translation to human patients have revealed that posttranslational modifications of individual proteins within NF-κB and hypoxia-inducible factor pathways serve as ideal targets for analysis in disease models. Studies defining differences and similarities between these responses have taught us a number of important lessons about the complexity of the inflammatory response. A clearer definition of these pathways has provided new insight into disease pathogenesis and, importantly, the potential for new therapeutic targets.
    MeSH term(s) Animals ; Humans ; Hydroxylation ; Hypoxia/complications ; Hypoxia/pathology ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Inflammatory Bowel Diseases/complications ; Inflammatory Bowel Diseases/pathology ; Intestinal Mucosa/pathology ; Protein Processing, Post-Translational
    Chemical Substances Hypoxia-Inducible Factor 1, alpha Subunit
    Language English
    Publishing date 2016-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1217870-6
    ISSN 1708-8267 ; 0009-9279 ; 1081-5589
    ISSN (online) 1708-8267
    ISSN 0009-9279 ; 1081-5589
    DOI 10.1097/JIM.0000000000000218
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Fundamental role for the creatine kinase pathway in protection from murine colitis.

    Hall, Caroline Ht / Lanis, Jordi M / Dowdell, Alexander S / Murphy, Emily M / Colgan, Sean P

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Inflammatory diseases of the digestive tract, including inflammatory bowel disease (IBD), cause metabolic stress within mucosal tissue. Creatine is a key energetic regulator. We previously reported a loss of creatine kinases (CKs) and the creatine ... ...

    Abstract Inflammatory diseases of the digestive tract, including inflammatory bowel disease (IBD), cause metabolic stress within mucosal tissue. Creatine is a key energetic regulator. We previously reported a loss of creatine kinases (CKs) and the creatine transporter expression in IBD patient intestinal biopsy samples and that creatine supplementation was protective in a dextran sulfate sodium (DSS) colitis mouse model. In the present studies, we evaluated the role of CK loss in active inflammation using the DSS colitis model. Mice lacking expression of CKB/CKMit (CKdKO) showed increased susceptibility to DSS colitis (weight loss, disease activity, permeability, colon length and histology). In a broad cytokine profiling, CKdKO mice expressed near absent IFN-γ levels. We identified losses in IFN-γ production from CD4
    Language English
    Publishing date 2023-06-09
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.06.07.544110
    Database MEDical Literature Analysis and Retrieval System OnLINE

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