GLORIA

GEOMAR Library Ocean Research Information Access

X

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
Filter
  • The American Association of Immunologists  (5)
Materialart
Verlag/Herausgeber
  • The American Association of Immunologists  (5)
Person/Organisation
Sprache
Erscheinungszeitraum
Fachgebiete(RVK)
  • 1
    Online-Ressource
    Online-Ressource
    Monocyte Chemoattractant Protein-1 Contributes to Gut Homeostasis and Intestinal Inflammation by Composition of IL-10–Producing Regulatory Macrophage Subset
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 5 ( 2010-03-01), p. 2671-2676
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 5 ( 2010-03-01), p. 2671-2676
    Kurzfassung: Lamina propria macrophages (LPMϕs) spontaneously produce large amounts of anti-inflammatory IL-10 and play a central role in regulation of immune responses against commensal bacteria. MCP-1 is a chemokine that plays an important role in recruitment of monocytes and macrophages to inflamed tissues. We demonstrated that, in addition to IL-10, LPMϕs produced large amounts of MCP-1, even in a steady state. MCP-1 deficiency caused impaired IL-10 production by LPMϕs and led to exacerbation of dextran sulfate sodium-induced acute colitis. As an explanation of this impaired IL-10 production by LPMϕs, we found that LPMϕs could be separated into two subsets with distinct side-scattered properties, namely LPMϕ1 (CD11b+F4/80+CD11c–SSChi) and LPMϕ2 (CD11b+F4/80+CD11c–SSClo). Unlike LPMϕ1, the LPMϕ2 subset migrated in response to MCP-1 and produced a larger amount of IL-10 in response to commensal bacteria. LPMϕs isolated from MCP-1–deficient mice produced less IL-10 as a consequence of the lack of the MCP-1–dependent LPMϕ2 population. This imbalanced composition in LPMϕ population may be involved in the susceptibility to DSS-induced colitis in MCP-1–deficient mice. Our results suggest that endogenous MCP-1 contributes to the composition of resident LPMϕ subsets in the intestine. Moreover, MCP-1–dependent LPMϕ2 subset may play an important role in maintenance of gut homeostasis in the steady state, and in the termination of excess inflammatory responses in the intestine, by producing IL-10.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.0804012
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2010
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Online-Ressource
  • 2
    Online-Ressource
    Online-Ressource
    The herbal medicine ‘Indigo naturalis’ altered gut microbiota to accumulate IL-22+ ILC3s
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 83.11-83.11
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 83.11-83.11
    Kurzfassung: Ulcerative colitis (UC) is a chronic inflammation of the large intestine led by the dysregulation of adaptive and innate immune responses. Recently, specific microbiota has been reported to instruct the immune cells and immune response. We have recently proved the clinical efficacy of “indigo naturalis (IN)”, a Chinese herbal medicine, on patients with UC by the multicenter randomized-controlled trial (INDIGO study, Gastroenterology 2018). 4%IN-fed mice ameliorated DSS-colitis (IN-DSS mice) compared to the normal diet-fed mice (ctrl-DSS mice). The number of IL-22+ ILC3s in the colonic lamina propria in IN-DSS mice increased more than the one in ctrl-DSS mice. We also confirmed that IN-fed diet mice significantly altered gut microbiota composition compared to the normal diet-fed mice. We next inoculated feces obtained from IN-fed mice or normal diet-fed mice to antibiotic treated mice (IN-FMT mice, ctrl-FMT mice respectively). Interestingly, IN-FMT mice significantly restored the pathology of DSS-induced colitis than ctrl-FMT mice with increased number of IL-22+ ILC3s. We showed IN induced specific microbiota which accumulated IL-22+ ILC3s in gut.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.83.11
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2020
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Online-Ressource
  • 3
    Online-Ressource
    Online-Ressource
    Enrichement of type I interferon signalling in the colonic ILC2 under inflammatory condition
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 1_Supplement ( 2023-05-01), p. 61.04-61.04
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 1_Supplement ( 2023-05-01), p. 61.04-61.04
    Kurzfassung: Group2 innate lymphoid cells (ILC2s) are known to contribute to a frontline defence against parasites and formation of allergic diseases, but little is known about the roles of ILC2s under intestinal inflammation including intestinal bowel diseases (IBD). In this study, we investigate the characteristics of ILC2s in health and colitis. Methods ILC2s were analysed in the mice with or without treatment of dextran sulphate sodium (DSS)-induced colitis, where surface markers and cytokine production was assessed by flow cytometry. The global gene expression of ILC2 in DSS-induced colitis and control mice were analysed by bulk RNA-sequencing (RNA-seq). Lastly, the mice was treated with anti-IFN-alpha/beta receptor1 (IFNAR1) antibody and then challenged to DSS-induced colitis. Results The number of ILC2s in the gastrointestinal tract was larger than that of spleen and liver in the healthy mice. At day 7 of DSS-induced colitis, IL-5 production from ILC2s was significantly reduced in flow cytometry data, and this was accompanied by enrichment of type I interferon (T1IFN) signalling in colitic ILC2 in RNA-seq data. Neutralisation of T1IFN signalling by anti-IFNAR antibody significantly increased severity of colitis. Conclusion Our data suggest that downregulation of Th2 cytokines and enrichment of T1IFN signatures in colitic ILC2s. T1IFN may stimulate ILC2 to induce colitis suppressive functions. This study was funded by the Japan Society for the Promotion of Science (JSPS) Grant-in-Aid for Transformative Research Areas(B): 21H05123; Advanced Research and Development Programs for Medical Innovation (AMED-CREST: 21gm1510002h0001, and 20gm1210001h0001; the Practical Research Project for Rare/Intractable Disease: 21ek0109556h0001)
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.210.Supp.61.04
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2023
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Online-Ressource
  • 4
    Online-Ressource
    Online-Ressource
    Intestinal barrier disruption inversely regulates liver inflammation via IL-10-producing macrophages
    The American Association of Immunologists ; 2017
    In:  The Journal of Immunology Vol. 198, No. 1_Supplement ( 2017-05-01), p. 221.2-221.2
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 198, No. 1_Supplement ( 2017-05-01), p. 221.2-221.2
    Kurzfassung: The gut-liver axis is a clinical topic as a potential therapeutic target of liver diseases. The interaction between microbial products and immune responses in the liver is still unknown. In the current study, we have demonstrated IL-10-producing CD11b+ F4/80+ macrophages contribute to immune tolerance in the inflamed liver under diminished intestinal barrier function in murine tandem model of dextran sulfate sodium (DSS)-colitis and Concanavalin A (ConA)-hepatitis. DSS-ConA mice with increased intestinal permeability developed less liver injury compared with DW-ConA mice. Of note, the severity of colitis was inversely correlated with subsequently induced liver injury. In DSS-ConA livers, increased CD11b+ macrophages showed regulatory characteristics with IL-10 production in vitro. Pretreatment with α-IL-10 antibody partially exacerbated the suppressed liver injury by DSS-ConA in vivo. Furthermore, pretreatment with CD11b+ macrophages derived from DSS-ConA livers protected mice from the subsequent liver injury. Mechanistically, we observed the contribution of gut microbiota, as the immunological tolerance induced by DSS-ConA is partially ablated by gut sterilization. Pretreatment with the portal serum derived from DSS-ConA mice partially protected mice from the subsequent liver injury. These results suggest that altered gut microbiota and the metabolites that pass through the portal vein with disrupted intestinal barrier directly gave rise to immunological permissiveness against the excessive stimulation in the liver. This study clarified the contribution of the gut-liver axis in the maintenance of immune balance in the liver and highlighted the microbiota as a potential therapeutic target for liver diseases.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.198.Supp.221.2
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2017
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Online-Ressource
  • 5
    Online-Ressource
    Online-Ressource
    New classification of CD4+CD8a+ double positive cells in Crohn’s disease patients
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 224.2-224.2
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 224.2-224.2
    Kurzfassung: The gastrointestinal tract absorbs nutrition while providing a defense response to foreign antigens including enteric bacteria or food. Once the antigen enter the intestine, inflammatory mononuclear cells are accumulated quickly, however some tissue resident T cells, such as regulatory T cells (Tregs) block the excessive tissue damage. We previously demonstrated that mouse CD4+CD8a+ double expressing (DP)cells and Tregs complementary play an immuno-suppressive role in IE and LP, and a part of IE DP cells is originally developed from Tregs in LP. However, DP cells are not well characterized in human especially in inflammatory bowel disease (IBD) patients. We obtained human small intestinal tissue from 9 colon cancer patients as normal tissue, and 5 Crohn’s disease(CD) patients, dividing into inflamed and non-inflamed lesion, and analysed by Flow cytometry. We confirmed DP cells are located in both IE and LP in human. First, we demonstrated the ratio of DP cells in normal tissue was as same as in non-inflamed lesion of CD patients. As we expected, the ratio of DP cells in inflamed tissue of CD patients was significantly decreased compared to normal tissue and non-inflamed lesion of CD. Then, we analysed the surface marker of Human DP cells. Surface staining of CD27 and CD45RA showed distinct difference between DP cells and the other CD4 T cells. DP cells expressed more memory T cell marker (CD27−CD45RA−) and less effector T cell marker (CD27+CD45RA−) than the other CD4 subset. Futher more, the more fraction of IE DP cells expressed CD103 than LP DP cells. Conclusively, these data indicated that human DP cell reside both in IE and LP and that DP cells are not a single characterized population, and the DP cells were decreased in inflamed lesion in CD.
    Materialart: Online-Ressource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.224.2
    RVK:
    XA 54100
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: The American Association of Immunologists
    Publikationsdatum: 2020
    ZDB Id: 1475085-5
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    Online-Ressource
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...