scholarly journals Expression of Concern for: Inhibition of CXCR4 by MicroRNA-1192 Reduces the Activation of Th17 Cells and Expression of Inflammation Factors in a Mouse Model of Vulvovaginal Candidiasis

2021 ◽  
Vol 55 (4) ◽  
pp. 538-538
Keyword(s):  
Mouse Model ◽  
Th17 Cells ◽  
Vulvovaginal Candidiasis

scholarly journals Xianfanghuomingyin, a Chinese Compound Medicine, Modulates the Proliferation and Differentiation of T Lymphocyte in a Collagen-Induced Arthritis Mouse Model

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Bo Nie ◽  
Xue Li ◽  
Yi Wei ◽  
Meng Chen ◽  
Jingwei Zhou ◽  
...  
Keyword(s):  
Mouse Model ◽  
Th17 Cells ◽  
Retinoic Acid Receptor ◽  
Treg Cells ◽  
Immunological Tolerance ◽  
Cartilage Destruction ◽  
Orphan Receptor ◽  
Th2 Cells ◽  
Collagen Induced Arthritis ◽  
Proliferation And Differentiation

In traditional Chinese medicine (TCM), xianfanghuomingyin (XFHM) is used to treat autoimmune diseases, including rheumatoid arthritis (RA). Here, we studied the mechanisms underlying its treatment effects, especially its anti-inflammatory effects in a collagen-induced arthritis (CIA) mouse model. We found that cartilage destruction and pannus formation were alleviated by treatment with XFHM. The abnormal differentiation of Th1 and Th17 cells was downregulated significantly by XFHM, and Th2 and Treg cells were upregulated. Moreover, the expression levels of specific cytokines and transcription factors related to Th1 cells (interferonγ[IFNγ], T-bet) and Th17 cells (interleukin- [IL-] 17) and the nuclear receptor retinoic acid receptor-related orphan receptor-gamma (RORγ) were downregulated. Serum IL-4 and GATA-3, which contribute to Th2 cells differentiation, increased significantly after XFHM administration. These results indicate that XFHM can restore the balance of T lymphocytes and reestablish the immunological tolerance to inhibit autoinflammatory disorder of RA. Taken together, XFHM can be used as a complementary or alternative traditional medicine to treat RA.

scholarly journals Differentiation of Pathogenic Th17 Cells Is Negatively Regulated by Let-7 MicroRNAs in a Mouse Model of Multiple Sclerosis

2020 ◽  
Vol 10 ◽  
Author(s):  
Constance C. Angelou ◽  
Alexandria C. Wells ◽  
Jyothi Vijayaraghavan ◽  
Carey E. Dougan ◽  
Rebecca Lawlor ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Mouse Model ◽  
Th17 Cells

IL-22 Is Critical To The Pathogenesis Of Cutaneous Gvhd Mediated By Th17 Cells

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4482-4482
Author(s):  
Hemamalini Bommiasamy ◽  
Laura Ott ◽  
Shelly West ◽  
LeShara M Fulton ◽  
Angela Panoskaltsis-Mortari ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Stem Cell ◽  
Mouse Model ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Th17 Cells ◽  
Acute Gvhd ◽  
Allogeneic Bone ◽  
Congenital Diseases

Background Allogeneic hematopoietic stem cell transplantation is used to treat a number of acquired and congenital diseases; however, a major complication of this therapy is graft versus host disease (GvHD). GvHD is a severe inflammatory disease caused by donor T cells recognizing host organs as foreign and mounting an immune response against them. Current treatment for GvHD is an immunosuppressive drug regimen that can predispose patients to opportunistic infections. Therefore, it is of critical importance to further understand the underlying mechanisms that mediate GvHD pathogenesis in efforts to develop novel therapeutic treatments. Previous work from our lab demonstrated that TH17 cells mediate severe cutaneous GvHD and that inhibiting IL-17 activity using a neutralizing anti-IL17 antibody was protective in a mouse model of skin GvHD. TH17 cells also produce the cytokine IL-22, which is known to be involved in skin inflammation resulting from psoriasis. We tested whether IL-22 from TH17 cells is also pathogenic in a mouse model of GvHD in which ex vivo polarized TH17 cells from B6 mice are transferred to lethally irradiated allogeneic B6D2 mice. Method B6D2 recipient mice were lethally irradiated with 900 cGy from a Cesium source. The following day recipient mice were given 3 x 106 T cell depleted bone marrow cells supplemented with 3-4 x 106 Th17 cells that had been polarized in vitro from fluorescence activated cell sorted CD4+/CD62Lhi T cells that had been cultured as described previously (Carlson et al Blood 2009). Recipient mice were followed for survival and scored for clinical GVHD using a standard scoring system. Additionally, recipient mice were evaluated clinically for cutaneous GVHD and scored for tissue pathology. GVHD organs were evaluated for the production of pro-inflammatory cytokines by ELISA and qPCR. Treated animals received control IgG or anti-IL-22 antibody (16mg/kg) weekly for four weeks starting on the day of transplant (Day 0). Results We found substantial expression of IL-22 mRNA in the skin of recipient mice who were transplanted with donor Th17 cells compared to those receiving naïve T cells alone (p< 0.05). When we evaluated the function of IL-22 produced by Th17 cells, we found a statistically significant decrease in cutaneous GVHD induced by Th17 cells in recipient animals treated with anti-IL-22 mAb (p< 0.05). While there was a decrease in cutaneous GVHD in the mice treated with anti-IL-22 mAb, there was no difference in overall survival or induction of GVHD outside of the cutaneous compartment. Additionally, we found increased expression of mRNA for IL-22 from a cohort of patients with late acute GVHD after allogeneic stem cell transplantation. Conclusions Unlike in the GI tract, the generation of IL-22 appears to play a pro-inflammatory role in the manifestation of cutaneous GVHD in mice after allogeneic bone marrow transplantation. High levels of mRNA for IL-22 were also found in the skin from a cohort of patients with late acute GVHD. These data suggest that targeting IL-22 may be beneficial in the treatment of cutaneous GVHD. Disclosures: Fouser: Pfizer: Employment.

The Dynamics Of Th17 Cells In A Cigarette Smoke Induced COPD Mouse Model

2012 ◽  
Author(s):  
Katrin Kohse ◽  
Gerrit John ◽  
Alexander Bohla ◽  
Oliver Eickelberg ◽  
Ali O. Yildirim
Keyword(s):  
Mouse Model ◽  
Cigarette Smoke ◽  
Th17 Cells

Th17 Cells Induce Dopaminergic Neuronal Death via LFA-1/ICAM-1 Interaction in a Mouse Model of Parkinson’s Disease

2016 ◽  
Vol 54 (10) ◽  
pp. 7762-7776 ◽  
Author(s):  
Zhan Liu ◽  
Yan Huang ◽  
Bei-Bei Cao ◽  
Yi-Hua Qiu ◽  
Yu-Ping Peng
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Neuronal Death ◽  
Th17 Cells

scholarly journals Distinct characteristics of hippocampal pathogenic TH17 cells in a mouse model of depression

2018 ◽  
Vol 73 ◽  
pp. 180-191 ◽  
Author(s):  
Eléonore Beurel ◽  
Jeffrey A. Lowell ◽  
Richard S. Jope
Keyword(s):  
Mouse Model ◽  
Th17 Cells

scholarly journals Inhibition of CXCR4 by MicroRNA-1192 Reduces the Activation of Th17 Cells and Expression of Inflammation Factors in a Mouse Model of Vulvovaginal Candidiasis

2018 ◽  
Vol 50 (3) ◽  
pp. 893-910 ◽  
Author(s):  
Jing Liu ◽  
Huai-Zhen Wang ◽  
Yong Sun
Keyword(s):  
Flow Cytometry ◽  
Epithelial Cells ◽  
Mouse Models ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Vulvovaginal Candidiasis ◽  
Inflammatory Factors ◽  
Cell Percentage ◽  
Vaginal Epithelial Cells ◽  
Protein Expressions

Background/Aims: Vulvovaginal candidiasis (VVC) is a disease commonly occurring in sexually active women. The involvement of microRNAs in several kinds of infectious diseases has been highlighted in a number of researches. Therefore, we conducted the present study in order to investigate whether microRNA-1192 (miR-1192) would significantly target CXCR4 in Th17 cells as well as inflammatory factors in mouse models suffering from VVC. Methods: Seventy-five mice were selected as test subjects for this study, of which twenty-five were used as the normal control, while the rest were treated with estradiol or oil-treated in order to establish VVC mouse models (each n = 25). Protein expressions of CXCR4, IL-6, IL-17, and IL-23 were all measured using both an immunohistochemistry and ELISA. The Th17 cell percentage in peripheral blood and the expression of RORγt in Th17 cells were detected using a flow cytometry. Mouse vaginal epithelial cells were isolated from normal mice, after which the mice were treated with estradiol to regulate their estrogen, followed by treatments involving the miR-1192 mimic, miR-1192 inhibitor, siRNA-CXCR4, and miR-1192 inhibitor + si-CXCR4. The cell cycle, apoptosis, and proliferation were all examined by using an additional flow cytometry as well as the employment of the MTT assay. The miR-1192, CXCR4, IL-6, IL-17, and IL-23 expressions in tissues and cells were both measured using both RT-qPCR and western blot assay techniques. Results: The mice treated with either estradiol or oil had presented to us lowered levels in miR-1192 expression as well as higher levels in both Th17 cell percentage and expression of RORγt in Th17 cells, along with mRNA and protein expressions of CXCR4, IL-6, IL-17, and IL-23. In cell experiments, the mouse vaginal epithelial cells that had been treated with miR-1192 inhibitor had shown us a decreased cell proliferation rate and contrarily increased expressions of CXCR4, IL-6, IL-17, and IL-23 mRNA, protein, and cell apoptosis rate; these results were opposite to the ones found in the mice treated with miR-1192 mimic. Conclusion: Our results provided significant evidence that miR-1192 could directly development and progression of VVC by restraining the CXCR4 gene in the VVC mice.

Sign in / Sign up

Export Citation Format

Share Document