Publications by authors named "Dahee Shim"

species include Meyer, L., , , , and , which contain bioactive components (BCs) such as ginsenosides and polysaccharides. Recently, growing evidence has revealed the pharmacological effects of species and their BCs on allergic airway diseases (AADs), including allergic asthma (AA) and allergic rhinitis (AR).

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In the wake of the COVID-19 pandemic, lung disorders have become a major health concern for humans. Allergic asthma is the most prevalent form of asthma, and its treatments target the inflammation process. Despite significant developments in the diagnosis and management of allergic asthma, side effects are a major concern.

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Article Synopsis
  • - The study investigates how high levels of lipids in the blood (hyperlipidemia) can trigger inflammation in the aortic valve, which is a key factor in the development of aortic valve disease, although the exact cellular processes involved are still uncertain.
  • - Researchers found a connection between low-density lipoprotein (LDL) and increased lipid and macrophage buildup in the aortic valve, using advanced techniques like single-cell RNA sequencing to analyze changes in various cell types during hyperlipidemia.
  • - Activation of the PPARγ pathway in valvular endothelial cells appears to play a protective role against inflammation in both mice and human aortic valves, suggesting that promoting this pathway could potentially reduce valvular inflammation related to
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Accumulating evidence suggests that two chronic respiratory diseases, nontuberculous mycobacterium (NTM)-pulmonary disease (PD) and allergic asthma, are frequently present together and that they likely influence the disease development and progression of each other. However, their precise interactions regarding the pathogenesis of comorbid diseases versus that of individual diseases are not well understood. In this study, comorbid diseases ( (Mav) pulmonary infection (PI) (Mav-PI) and ovalbumin-induced allergic asthma) were established in mice in different orders and at different time periods.

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(Mtb) causes chronic granulomatous lung disease in humans. Recently, novel strategies such as host-directed therapeutics and adjunctive therapies that enhance the effect of existing antibiotics have emerged to better control Mtb infection. Recent advances in understanding the metabolic interplay between host immune cells and pathogens have provided new insights into how their interactions ultimately influence disease outcomes and antibiotic-treatment efficacy.

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Dendritic cells (DCs) are the main mediators of Th2 immune responses in allergic asthma, and Fms-like tyrosine kinase 3 ligand (Flt3L) is an important growth factor for the development and homeostasis of DCs. This study identified the DC populations that primarily cause the initiation and development of allergic lung inflammation using Fms-like tyrosine kinase 3 (Flt3) knockout (KO) mice with allergen-induced allergic asthma. We observed type 2 allergic lung inflammation with goblet cell hyperplasia in Flt3 KO mice, despite a significant reduction in total DCs, particularly CD103 DCs, which was barely detected.

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Background: Macrophages produce many inflammation-associated molecules, released by matrix metalloproteinases, such as adhesion molecules, and cytokines, as well, which play a crucial role in atherosclerosis. In this context, we investigated the relationship between Ninjurin-1 (Ninj1 [nerve injury-induced protein]), a novel matrix metalloproteinase 9 substrate, expression, and atherosclerosis progression.

Methods: Ninj1 expression and atherosclerosis progression were assessed in atherosclerotic aortic tissue and serum samples from patients with coronary artery disease and healthy controls, and atheroprone apolipoprotein e-deficient () and wild-type mice, as well.

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Tuberculosis (TB) is a leading cause of death worldwide following infection with (Mtb), with 1.5 million deaths from this disease reported in 2018. Once the bacilli are inhaled, alveolar and interstitial macrophages become infected with Mtb and differentiate into lipid-laden foamy macrophages leading to lung inflammation.

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Purpose: Simple and reliable animal models of human diseases contribute to the understanding of disease pathogenesis as well as the development of therapeutic interventions. Although several murine models to mimic human asthma have been established, most of them require anesthesia, resulting in variability among test individuals, and do not mimic asthmatic responses accompanied by T-helper (Th) 17 and neutrophils. As dendritic cells (DCs) are known to play an important role in initiating and maintaining asthmatic inflammation, we developed an asthma model via adoptive transfer of allergen-loaded DCs.

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To this date, the criteria to distinguish peritoneal macrophages and dendritic cells (DCs) are not clear. Here we delineate the subsets of myeloid mononuclear cells in the mouse peritoneal cavity. Considering phenotypical, functional, and ontogenic features, peritoneal myeloid mononuclear cells are divided into 5 subsets: large peritoneal macrophages (LPMs), small peritoneal macrophages (SPMs), DCs, and 2 MHCIICD11cCD115 subpopulations (i.

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Rationale: Monocyte infiltration into the subintimal space and its intracellular lipid accumulation are the most prominent features of atherosclerosis. To understand the pathophysiology of atherosclerotic disease, we need to understand the characteristics of lipid-laden foamy macrophages in the subintimal space during atherosclerosis.

Objective: We sought to examine the transcriptomic profiles of foamy and nonfoamy macrophages isolated from atherosclerotic intima.

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Dendritic cells (DCs) are central to initiate antigen-specific immunity and tolerance. The in vivo development and distribution of DCs are now better understood even in nonlymphoid tissues [1]. Atherosclerosis is a chronic inflammatory disease of blood vessels and DCs are highly enriched in the intimal area of the aorta, which is predisposed to develop atherosclerosis.

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Background: Allergic rhinitis (AR) is the most common allergic disease but little is known about the difference of local immune responses in children and adults with AR.

Objective: To compare local immune responses between children and adults with AR and nonallergic rhinitis (NAR), and to investigate whether the association of local and systemic immune responses is different between the two age groups.

Methods: Fifty-one patients with chronic rhinitis were enrolled and grouped into children (N = 27, mean age 7.

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Article Synopsis
  • Plasmacytoid dendritic cells (pDCs) are specialized immune cells that produce type I interferon and help promote tolerance in T cells, particularly during inflammation.
  • This study discovered that pDCs are present in the aortic intima and that their removal in mice worsened atherosclerosis, indicating their important role in the disease.
  • The research demonstrated that pDCs promote the development of regulatory T cells (Tregs) in the aorta, and their absence leads to reduced Treg numbers and IL-10, revealing a protective mechanism against atherosclerosis.
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Resistin-like molecule alpha (Retnla), also known as 'Found in inflammatory zone 1', is a secreted protein that has been found in bronchoalveolar lavage (BAL) fluid of ovalbumin (OVA)-induced asthmatic mice and plays a role as a regulator of T helper (Th)2-driven inflammation. However, the role of Retnla in the progress of Th2-driven airway inflammation is not yet clear. To better understand the function of Retnla in Th2-driven airway inflammation, we generated Retnla-overexpressing (Retnla-Tg) mice.

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