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  • 1
    Online Resource
    Online Resource
    Targeting AhR as a Novel Therapeutic Modality against Inflammatory Diseases
    MDPI AG ; 2021
    In:  International Journal of Molecular Sciences Vol. 23, No. 1 ( 2021-12-28), p. 288-
    Details
    In: International Journal of Molecular Sciences, MDPI AG, Vol. 23, No. 1 ( 2021-12-28), p. 288-
    Abstract: For decades, activation of Aryl Hydrocarbon Receptor (AhR) was excluded from consideration as a therapeutic approach due to the potential toxic effects of AhR ligands and the induction of the cytochrome P450 enzyme, Cyp1a1, following AhR activation. However, it is now understood that AhR activation not only serves as an environmental sensor that regulates the effects of environmental toxins, but also as a key immunomodulator where ligands induce a variety of cellular and epigenetic mechanisms to attenuate inflammation. Thus, the emergence of further in-depth research into diverse groups of compounds capable of activating this receptor has prompted reconsideration of its use therapeutically. The aim of this review is to summarize the body of research surrounding AhR and its role in regulating inflammation. Specifically, evidence supporting the potential of targeting this receptor to modulate the immune response in inflammatory and autoimmune diseases will be highlighted. Additionally, the opportunities and challenges of developing AhR-based therapies to suppress inflammation will be discussed.
    Type of Medium: Online Resource
    ISSN: 1422-0067
    URL: Article
    DOI: 10.3390/ijms23010288
    Language: English
    Publisher: MDPI AG
    Publication Date: 2021
    detail.hit.zdb_id: 2019364-6
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  • 2
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    Altered Gut DNA virome diversity associated HMGB1 release regulates reactive Astrocytes-induced IL6 release preferably via TLR4-NFkB pathway in experimental Gulf War Illness
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 64.15-64.15
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 64.15-64.15
    Abstract: In a recent study, we showed that the gut DNA bacteriophage dysbiosis in Gulf War Illness (GWI) was strongly associated with compromised intestinal epithelial cell integrity, increased circulatory IL6 and neuroinflammation. The current study further investigates the mechanism of DNA bacteriophage-IL6 axis in neuroinflammation. Advancing the previous findings, we show that viral dysbiosis positively correlated with high mobility group box protein 1 (HMGB1; a damage-associated molecular pattern) expression and release in circulation following GWI induction in mice. The circulatory HMGB1 activated brain Astrocytes via altering brain endothelial tight junction proteins and crossing the blood-brain barrier. Interestingly, both in GWI mice and mouse primary Astrocytes cell culture showed an increased brain IL6 mRNA and subsequent protein expression. However, GWI mice treated with Ribavirin (used for partial gut viral sterility) showed decreased intestinal HMGB1 and brain IL6 expression. Mechanistically, HMGB1 activated innate immune response via IRAKs-IKKα-NFkB instead of either RAGE-MAPK or PI3K-mTOR pathway. Surprisingly, inhibition of RAGE or PI3K pathway in HMGB1 primed mouse Astrocyte cells showed a significant increase in IL6 expression and release suggesting NFkB activation as a preferential pathway in GWI-Astrocyte-induced IL6 release. In summary, GWI-associated gut viral dysbiosis associated intestinal HMGB1 release activates brain Astrocytes and IL6 release via toll-like receptor 4-NFkB dependent pathway, thus causing neuroinflammation in GWI. The above mechanism can form a basis for studying inflammation-associated neurocognitive abnormalities in GWI.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.64.15
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 3
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    Production of MHCII ‐expressing classical monocytes increases during aging in mice and humans
    Wiley ; 2022
    In:  Aging Cell Vol. 21, No. 10 ( 2022-10)
    Details
    In: Aging Cell, Wiley, Vol. 21, No. 10 ( 2022-10)
    Abstract: Aging is associated with increased monocyte production and altered monocyte function. Classical monocytes are heterogenous and a shift in their subset composition may underlie some of their apparent functional changes during aging. We have previously shown that mouse granulocyte‐monocyte progenitors (GMPs) produce “neutrophil‐like” monocytes (NeuMo), whereas monocyte‐dendritic cell progenitors (MDPs) produce monocyte‐derived dendritic cell (moDC)‐producing monocytes (DCMo). Here, we demonstrate that classical monocytes from the bone marrow of old male and female mice have higher expression of DCMo signature genes ( H2‐Aa , H2‐Ab1 , H2‐Eb1 , Cd74 ), and that more classical monocytes express MHCII and CD74 protein. Moreover, we show that bone marrow MDPs and classical monocytes from old mice yield more moDC. We also demonstrate higher expression of Aw112010 in old monocytes and that Aw112010 lncRNA activity regulates MHCII induction in macrophages, which suggests that elevated Aw112010 levels may underlie increased MHCII expression during monocyte aging. Finally, we show that classical monocyte expression of MHCII is also elevated during healthy aging in humans. Thus, aging‐associated changes in monocyte production may underlie altered monocyte function and have implications for aging‐associated disorders.
    Type of Medium: Online Resource
    ISSN: 1474-9718 , 1474-9726
    URL: Issue
    URL: Article
    DOI: 10.1111/acel.v21.10
    DOI: 10.1111/acel.13701
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2099130-7
    SSG: 12
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  • 4
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    2,3,7,8-Tetrachlorodibenzo-p-dioxin Induces Gimap5 Expression to Ameliorate Concanavalin-Induced T Cell-Mediated Liver Injury
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 154.13-154.13
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 154.13-154.13
    Abstract: GTPase of the immune-associated protein 5 (Gimap5) has been implicated in immune cell maintenance and development. A mouse model comparable to autoimmune hepatitis in humans was used to study the alterations induced in the gene expression profile of immune cells upon administration of environmental toxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD). In this study, we tested the hypothesis that TCDD is capable of modulating gene expression to ameliorate autoimmune hepatitis severity. Mice were injected intravenously with 12.5 mg/kg concanavalin A (ConA) and treated intraperitoneally one hour after challenge with vehicle or 10 μg/kg TCDD. TCDD-treated mice showed lower levels of liver injury enzymes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), as compared to vehicle-treated mice. Histopathological analysis revealed a reduction in liver damage in the TCDD-treated group as compared to the vehicle-treated control. Furthermore, flow cytometric analysis of liver-infiltrating mononuclear cells demonstrated that following treatment with TCDD, there was an increase in FoxP3+CD4+ Tregs as well as a decrease in proinflammatory Tbet+ Th1 and RORγt+ Th17 T helper cell subtypes after induction of the disease. Single cell RNA-sequencing was conducted on liver mononuclear cells to further assess the changes induced by TCDD. The gene expression profile showed that TCDD treatment significantly upregulated the expression of vital genes such as Gimap5, a maintenance gene for normal liver function and survival of T cells. In summary, our data suggests that TCDD is capable of inducing Gimap5 expression in autoimmune hepatitis, which in turn modulates the progression of this disease.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.154.13
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 5
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    Treatment with natural AhR ligand leads to amelioration of LPS-induced acute lung injury by decreasing microRNA 29b-2-5p expression targeting increased IL-22 production
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 79.1-79.1
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 79.1-79.1
    Abstract: Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) are severe pulmonary inflammatory diseases that cause destruction and remolding of the lung epithelial barrier, which may lead to restriction of pulmonary functionality and/or death. Indole-3-carbinol (I3C), a naturally occurring Ahr ligand has been shown to ameliorate multiple inflammatory disorders. Our studies are aimed at determining whether treatment with the I3C affects reparative reepithelialization and restores lung functioning through an immune-mediated mechanism. Towards this, 5mg/kg of LPS was intranasally injected in C57BL/6 mice to induce ALI. Three hours following LPS administration, the mice were treated with 40mg/kg I3C. After 48 hours, we examined lung functions using Buxco plethysmography and noticed LPS + I3C treated-mice have similar functionality as naïve mice in multiple parameters including ratio of time peak expiratory flow (Rpef), rejection index (Rinx), and tidal volume (TV) basal pulmonary functions whereas LPS+vehicle treated mice showed alterations. Histopathological analysis revealed fibrotic tissue in lung sections of LPS + Vehicle administered mice, but not in LPS + I3C treated mice. In addition, I3C increased the expression of Th22 (CD3+CD4+IL22+) cells, which are key mediators of epithelial cell layer protection, antimicrobial peptide production, and reepithelialization improvement. I3C increased IL-22 expression in bronchoalveolar lavage fluid, and decreased the expression in miR-29b-2-5p transcript that directly regulates IL-22 expression. In conclusion, our studies suggest that Ahr ligand I3C alleviates lung injury by maintaining lung epithelium integrity which may be mediated by IL-22 secreting T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.79.1
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 6
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    Epigenetic regulation of C-Kitlo FcɛR1a+ mast cells by cannabidiol during staphylococcal enterotoxin B-induced liver injury
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 152.7-152.7
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 152.7-152.7
    Abstract: Although recent studies have established cannabidiol (CBD) as a potent anti-inflammatory agent, the mechanisms governing these processes remain unclear. Our previous research demonstrated that CBD treatment induced expansion of CD11b+Gr-1+MDSC in the peritoneum, which suppressed T cell functions leading to attenuation of staphylococcal enterotoxin B (SEB)-mediated liver inflammation in mice. Using the same model, we characterize the effects of CBD administration in the liver. Briefly, mice were injected intraperitoneally (I.P.) with 50mg/kg of CBD for 4 days (d), followed by SEB challenge on d 3. Flow cytometry analysis revealed a significant reduction in Vβ8+ CD8+ T cells. In agreement with our earlier findings, mice treated with CBD displayed robust expansion of Gr-1+ MDSC in the liver, which was primarily comprised of Ly6CHI MHCIILO leukocytes. As mast cells have been found to play a role in CBD-mediated induction of MDSC via increased peroxisome proliferator-activated receptor gamma (PPARγ) signaling, we examined changes to liver mast cell populations. We discovered two distinct subsets of mast cells, C-KithiFcɛR1a+ and C-Kitlo FcɛR1a+present in the liver. CBD treatment promoted expansion of the C-Kitlo FcɛR1a+ subset. Analysis by miRNA microarray displayed enrichment of miRNAs targeting mast cell growth factor, KIT ligand (KITLG), and significant downregulation of miR-217-5p, which is conserved for the co-activator of PPARγ (PPARγC1A). Increased gene expression of PPARγ was confirmed by single-cell RNA sequencing (sc-RNAseq). Taken together, our results identify CBD induced epigenetic reduction of C-Kit expression and KITLG signaling in mast cells to favor PPARγ signaling as a novel anti-inflammatory mechanism.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.152.7
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 7
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    Resveratrol Downregulates miR‐31 to Promote T Regulatory Cells during Prevention of TNBS‐Induced Colitis
    Wiley ; 2020
    In:  Molecular Nutrition & Food Research Vol. 64, No. 1 ( 2020-01)
    Details
    In: Molecular Nutrition & Food Research, Wiley, Vol. 64, No. 1 ( 2020-01)
    Abstract: Colitis, an inflammatory bowel disease, is associated with aberrant regulation of the colonic mucosal immune system. Resveratrol, a natural plant product, has been found to exert anti‐inflammatory properties and attenuate the development of murine colitis. In the current study, the role of microRNA (miR) in the ability of resveratrol to suppress colonic inflammation is examined. Methods and results BALB/C mice with 2,4,6‐Trinitrobenzenesulfonic acid solution (TNBS)‐induced colitis, when treated with resveratrol, show improved clinical outcomes and reduce induction of inflammatory T cells (Th17 and Th1) while increasing CD4+Foxp3+ regulatory T cells (Tregs) and IL‐10‐producing CD4+ T cells. miR microarray analysis and polymerase chain reaction (PCR) validation from CD4+ T cells show treatment with resveratrol decreases the expression of several miRs (miR‐31, Let7a, miR‐132) that targets cytokines and transcription factors involved in anti‐inflammatory T cell responses (Foxp3 and TGF‐β). Transfection studies with miR‐31 confirm that this miR directly regulates the expression of Foxp3. Lastly, analysis of public data from human patients with ulcerative colitis reveals that miR‐31 expression is significantly increased when compared to controls. Conclusion Together, the current study demonstrates that resveratrol‐mediated attenuation of colitis may be regulated by miR‐31 through induction of Tregs and miR‐31 may serve as a therapeutic target for human colitis.
    Type of Medium: Online Resource
    ISSN: 1613-4125 , 1613-4133
    URL: Issue
    URL: Article
    DOI: 10.1002/mnfr.v64.1
    DOI: 10.1002/mnfr.201900633
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2160372-8
    SSG: 12
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  • 8
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    Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22–dependent manner
    American Society for Clinical Investigation ; 2020
    In:  JCI Insight Vol. 5, No. 1 ( 2020-1-16)
    Details
    In: JCI Insight, American Society for Clinical Investigation, Vol. 5, No. 1 ( 2020-1-16)
    Type of Medium: Online Resource
    ISSN: 2379-3708
    URL: Article
    URL: Article
    DOI: 10.1172/jci.insight.127551
    DOI: 10.1172/jci.insight.127551DS1
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 2020
    detail.hit.zdb_id: 2874757-4
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  • 9
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    B cells regulate luminal bile acid composition in the small intestine
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 1_Supplement ( 2023-05-01), p. 228.02-228.02
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 1_Supplement ( 2023-05-01), p. 228.02-228.02
    Abstract: Recent studies have demonstrated that bile acids (BA) influence immune cell homeostasis in the gut. However, whether and how, the host immune response can influence BA biochemistry is unknown. This is an important question to answer because small shifts in BA composition in the gut can have significant pathophysiological consequences. Previously, we have demonstrated that CD19 −/−mice, which have a defect in B cell activation and consequently an aberrant humoral immune response, develop a small intestine (SI) enteropathy that is associated with abnormal luminal BA composition. However, CD19 −/−mice are not B-cell-deficient and present with multiple aberrant immune phenotypes. Here, we used B cell-deficient JHminus;/minus; mice to more effectively define this interaction. Results of our experiments provide three key observations. First, J H−/−mice develop altered SI BA pools compared to their WT littermates. Second, adoptive transfer of WT B cells into neonatal J H−/−mice led to the development of normal BA pools and rescued mice from SI enteropathy. Third, adoptive transfer of B cells incapable of secreting IgA into neonatal J H−/−mice failed to restore normal bile acid composition and only moderately protected animals from developing SI enteropathy. Collectively, the results of our experiments clearly demonstrate that B cells regulate bile acid composition in the SI and that the synthesis of mucosal IgA may be particularly important for driving this effect.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.210.Supp.228.02
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2023
    detail.hit.zdb_id: 1475085-5
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  • 10
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    Regulation of macrophages in tumor microenvironment by microRNA in T cell lymphoma-bearing mice
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 204, No. 1_Supplement ( 2020-05-01), p. 164.18-164.18
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 204, No. 1_Supplement ( 2020-05-01), p. 164.18-164.18
    Abstract: The tumor microenvironment is a complex niche created by cancer cells to survive and evade the immune system. Macrophages (Mϕs) are considered to be one of the most abundant cells in the cancer microenvironment. Studies have shown that cancer cells have predilection for the M2 cell phenotype compared to M1 in the microenvironment, because M2 Mϕs promote immunosuppression and subsequently enhance tumor cell proliferation and angiogenesis. The aim of this study was to compare the gene expression profile of tumor-associated Mϕs (TAMs) and splenic Mϕs from tumor-bearing hosts (TBHs) and determine the epigenetic regulation of altered genes. For this purpose, C57BL/6 mice were injected with 1×106 EL4 cancer cells subcutaneous to induce tumor growth and 10 days later, TAMs and splenic Mϕs were isolated. Cell phenotyping by flow cytometry showed that there was an increase in M2 cells in TAMs when compared to splenic Mϕs in TBHs. TAMs also exhibited increase in IL-10, IL-6, VEGFA, and ARG-1 whereas there was a decrease in the expression of MYD88, PTEN, TGFβ3 and P53 when compared to splenic Mϕs in TBHs. Analysis of the microRNA profile of the Mϕs showed differential regulation and using ingenuity pathway analysis (IPA), we found various miRs (miR-21a, miR-30a, miR-30c, miR-125b, miR-155) were upregulated. These miRs targeted MYD88, PTEN and P53, which leads to the overexpression of IL10, known to skew Mϕ polarization to an M2 phenotype. In summary, these studies demonstrate that several miRs regulate IL10 to polarize TAMs from an M1 to M2 phenotype in the tumor microenvironment. (Supported by NIH P01AT003961, P20GM103641, R01AI129788, R01 ES030144 and R01AI123947)
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.204.Supp.164.18
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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