Background: Few satisfactory animal models of laryngopharyngeal reflux (LPR) is available. Interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) may be associated with the pathogenesis of LPR injuries and laryngeal carcinomas.
Objectives: To establish an animal model of LPR and to explore the related pathological changes and cytokine expression in the vocal cord tissue.
Methods: Twenty rabbits were divided into experimental and control groups. Dilatation of the upper and lower esophageal sphincter were carried out in the experimental group. The pH of the pharynx, pathological, and ultrastructural changes of the laryngeal tissue, and expression of IL-8 and VEGF were compared between the experimental group and controls.
Results: pH monitoring results and the dilated intercellular space of the vocal cord mucosa showed that the experimental group developed laryngopharyngeal reflux. There were significant differences in the immunohistochemical staining scores of both IL-8 (P = 0.015) and VEGF (P = 0.007) between the experimental and control groups in the vocal cord tissue.
Conclusions: We successfully established a model of LPR, showing histopathological and ultrastructural changes consistent with the disease. The expression of IL-8 and VEGF may increase during the pathogenesis of LPR.
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http://dx.doi.org/10.1016/j.jvoice.2020.01.021 | DOI Listing |
Nan Fang Yi Ke Da Xue Xue Bao
December 2024
Department of Rheumatology and Immunology, First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Objectives: To explore the mechanism of Granules (QJZG) for improving thrombocytopenia in a mouse model of systemic lupus erythematosus (SLE).
Methods: Twenty-four MRL/lpr lupus mice were randomized equally into 4 groups for treatment with daily gavage of saline, QJZG or prednisone (Pred) or intraperitoneal injection (twice a week) of CaMKK2 activator, with 6 C57BL/6 mice with saline gavage as the control group. After 8 weeks of treatment, the mice were examined for PLT, PCT, PDW, MPV, serum levels of TPO, IL-6, IL-10, TNF-α and IFN-γ, and calcium ion fluorescence intensity using ELISA or flow-through assay.
Phospholipase A2 receptor 1 (PLA2R1) exists important role in membranous nephropathy. In this study, we evaluate a PLA2R1 in a middle-aged rat model of renal function repair to further investigate the molecular mechanisms of membranous nephropathy. We analyzed the PLA2R1 knockout (KO) model and PLA2R1 knock in (KI) model in rats, extending the time to 85 weeks of age.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
College of Pharmacy, Chungbuk National University, Chungbuk 28160, Republic of Korea.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by autoantibody production by hyper-activated B cells. Although mesenchymal stem cells (MSCs) relieve lupus symptoms by inhibiting mainly T cells, whether MSCs also inhibit B cells has been controversial. Here, we found that naïve MSCs inhibited IFN-γ production by T cells, but not IgM production by B cells.
View Article and Find Full Text PDFFASEB J
December 2024
Department of Nephrology, Hunan Clinical Research Center for Chronic Kidney Disease, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Hunan, People's Republic of China.
Tubulointerstitial injury has been increasingly recognized as an important component in lupus nephritis (LN) pathology over the last decades. However, current clinical treatment options for this process remain limited. In this study, we aimed to investigate the potential benefits of GS-4997, a selective inhibitor of ASK1, in tubulointerstitial injury of LN.
View Article and Find Full Text PDFRheumatology (Oxford)
December 2024
Division of Rheumatology, Department of Medicine, Mayo Clinic Rochester, MN, USA.
Objective: We aim to explore the role of mechanistic target of rapamycin complex (mTORC) 2 in systemic lupus erythematosus (SLE) development, the in vivo regulation of mTORC2 by type I interferon (IFN) signaling in autoimmunity, and to use mTORC2 targeting therapy to ameliorate lupus-like symptoms in an in vivo lupus mouse model and an in vitro coculture model using human PBMCs.
Method: We first induced lupus-like disease in T cell specific Rictor, a key component of mTORC2, deficient mice by topical application of imiquimod (IMQ) and monitored disease development. Next, we investigated the changes of mTORC2 signaling and immunological phenotypes in type I IFNAR deficient Lpr mice.
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