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  • The American Association of Immunologists  (4)
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  • The American Association of Immunologists  (4)
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  • 1
    Online Resource
    Online Resource
    4-Ethylguaiacol modulates neuroinflammation and Th1/Th17 differentiation to ameliorate disease severity in experimental autoimmune encephalomyelitis
    The American Association of Immunologists ; 2021
    In:  The Journal of Immunology Vol. 206, No. 1_Supplement ( 2021-05-01), p. 18.08-18.08
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 206, No. 1_Supplement ( 2021-05-01), p. 18.08-18.08
    Abstract: Multiple sclerosis (MS) is a progressive autoimmune disease characterized by the accumulation of pathogenic inflammatory immune cells in the central nervous system (CNS) that subsequently causes focal inflammation, demyelination, and neuronal damage. Experimental Autoimmune Encephalomyelitis (EAE) is a well-established murine model of MS. Presently, growing evidences show that phenolic compounds exert anti-inflammatory effects by inhibiting the production of inflammatory molecules. 4-ethylguaiacol (4-EG), a phenolic compound, which was detected in foods, such as green bell peppers, corns, sesames, and coffee has been shown to possess anti-inflammatory effects through attenuating peripheral immune responses. However, whether 4-EG exerts anti-inflammatory effects on modulating the CNS inflammatory immune responses remains unexplored. In this study we assessed the therapeutic effect of 4-EG in EAE using both chronical and relapsing-remitting animal models. Our results showed that 4-EG not only ameliorated disease severity in chronic EAE but also mitigated disease progression in relapsing-remitting EAE. Further investigations revealed that 4-EG suppressed MG activation, inhibited Th1 and Th17 infiltration, and mitigated BBB disruption in the CNS of EAE. Furthermore, 4-EG suppressed Th1 and Th17 differentiation in the periphery of EAE. Finally, 4-EG induced HO-1 expression in the CNS of EAE as well as in MG and macrophages. In summary, our work demonstrates for the first time that 4-EG confers a protection against autoimmune disease EAE through modulating neuroinflammation and inhibiting Th1/Th17 differentiation, suggesting that 4-EG could be developed as a therapeutic agent for the treatment of MS/EAE.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.206.Supp.18.08
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2021
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Single-cell transcriptome profiling reveals heterogeneity of brain myeloid cells and unique subsets that regulate T cell immunity and cerebrovascular inflammation in diet-induced obesity
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 69.4-69.4
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 69.4-69.4
    Abstract: Midlife obesity and type 2 diabetes mellitus (T2DM) are linked to decreased cognition and strong risk for Alzheimer’s disease in late life. Previous studies show that obesity/T2DM is associated with a heightened state of neuroinflammation in aging mice. However, it remains unclear how diverse immune cell populations in the brain contribute to the cognitive decline. To address this, we fed middle-aged mice with high-fat diet (HFD) to induce visceral obesity and hyperglycemia. Chronic HFD consumption resulted in cognitive impairment and activation of brain resident microglia (MG). The CD45hiCD11b+ peripheral myeloid cells and CD3+ T cells were significantly increased in the brain of obese mice. Single-cell RNA sequencing was performed to characterize CD11b+ cells isolated from the brain. Unsupervised clustering singled out distinct myeloid cell clusters. Using Tmem119 and P2ry12 as markers to distinguish MG from infiltrating cells, we observed a 2-fold increase of peripheral myeloid cells, comprising distinct clusters in HFD-fed mice. Multiple subsets of MG were identified in HFD-fed mice, showing Ms4a, Apoe and gene signatures of perivascular macrophages. Notably, these subsets expressed high levels of MHC class-II-related molecules, H2-Eb1, H2-Ab1, and Cd74, and with special functions in lipid metabolism. These data suggested possible interactions between MG and T cells to potentiate neuroinflammation in HFD-fed mice. Overall, our results highlighted heterogeneity of brain myeloid cells in obesity during aging. The identified subsets of MG provide insights into brain MG controlling T cell immunity and cerebrovascular inflammation, which might lead to cognitive impairment associated with obesity and T2DM during aging.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.69.4
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
    Location Call Number Limitation Availability
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Dimethyl Itaconate, an Itaconate Derivative, Exhibits Immunomodulatory Effects on Neuroinflammation in Experimental Autoimmune Encephalomyelitis
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 160.9-160.9
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 160.9-160.9
    Abstract: Itaconate has recently emerged as a regulator of immune cell function. Studies show that itaconate is required for the activation of anti-inflammatory transcription factor Nrf2 by LPS in macrophages. Moreover, dimethyl itaconate (DMI), an itaconate derivative, has been shown to inhibit IL-17-induced IκBζ activation in keratinocytes and modulate IL-17-IκBζ pathway-mediated skin inflammation in an animal model of psoriasis. Currently, the effect of itaconate on regulating macrophage functions and peripheral inflammatory immune responses is well established. However, its effect on microglia (MG) and CNS inflammatory immune responses remains unexplored. Thus, in this study we investigated whether itaconate possesses an immunomodulatory effect on regulating MG activation and CNS inflammation in experimental autoimmune encephalomyelitis (EAE). Chronic C57BL/6 EAE and relapsing-remitting SJL/J EAE were induced to assess the therapeutic effect of DMI. Our results show DMI ameliorated disease severity in the chronic C57BL/6 EAE model. Further analysis of the cellular and molecular mechanisms revealed that DMI mitigated blood-brain barrier disruption, inhibited MMP3 and MMP9 production, suppressed microglia activation, and repressed CNS infiltration of Th1 and Th17 cells. Strikingly, DMI also exhibited a therapeutic effect on lessening severity of relapse in the relapsing-remitting SJL/J EAE model. In conclusion, we demonstrate for the first time that DMI suppressed neuroinflammation and ameliorated disease severity in EAE through multiple cellular and molecular mechanisms, and our findings suggest that DMI can be developed as a novel therapeutic agent for the treatment of EAE through its anti-inflammatory properties.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.160.9
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
    Location Call Number Limitation Availability
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Immunoresponsive gene 1 modulates neuroinflammation through the induction of heme oxygenase-1
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 208, No. 1_Supplement ( 2022-05-01), p. 111.02-111.02
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 208, No. 1_Supplement ( 2022-05-01), p. 111.02-111.02
    Abstract: Inflammatory stimuli induce immunoresponsive gene 1 (IRG1) expression that in turn catalyzes the production of itaconate through diverting cis-aconitate away from the tricarboxylic acid cycle. The immunoregulatory effect of IRG1/itaconate axis has been recently documented in lipopolysaccharide-activated mouse and human macrophages. Currently, whether IRG1/itaconate axis exerts a modulatory effect in ischemic stroke remains unexplored. In this study, we investigated whether IRG1 plays a role in modulating ischemic brain injury. Our results showed IRG1 was highly induced in the ischemic brain following ischemic injury. We found that IRG1−/− stroke animals exhibited exacerbated brain injury, displayed with enlarged cerebral infarct, compared to wild type stroke controls. Furthermore, IRG1−/− stroke animals presented aggravated blood-brain barrier disruption, associated with augmented Evans blue leakage of the ischemic brain. Moreover, IRG1−/− stroke animals displayed elevated microglia activation, demonstrated with increased CD68, CD86, and Iba1 expression. Further analysis revealed that IRG1 was induced in microglia after ischemic stroke, and deficiency in IRG1 resulted in repressed microglial heme oxygenase-1 (HO-1) expression. Notably, the administration of dimethyl itaconate, an itaconate derivative, to compensate the deficiency of IRG1/itaconate axis led to enhanced microglial HO-1 expression, alleviated ischemic brain injury, improved motor function, and decreased mortality rate in IRG1−/− stroke animals. In summary, we demonstrate that the induction of IRG1 in microglia following ischemic stroke may serve as a protective mechanism to restrain brain injury through HO-1 upregulation. This work was supported by Indiana University Startup Fund and in part by the National Institutes of Health (R01NS102449) to J.-H.Y.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.208.Supp.111.02
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
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