Publications by authors named "Sachiko Yamaguchi"

Adipose-derived stem cell (ASC)-released exosomes (ASCexos) have multiple biological activities. We examined the effect of ASCexos derived from the inguinal adipose tissue of exercise-trained rats (EX-ASCexos) on adipogenic conversion of 3T3-L1 cells and analyzed their microRNA (miRNA) expression profiles. Differentiation of 3T3-L1 cells into adipocytes was performed for 9 d with EX-ASCexos or ASCexos from sedentary control rats (SED-ASCexos), and the expression of proteins and miRNA involved in adipogenic differentiation were determined.

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  • Severely immunodeficient mice are valuable for researching tumors and therapeutic agents, as well as studying human viral infections when engrafted with human cells.
  • The study identified a unique immunodeficient mouse strain with a mutation in the Prkdc gene that has poor immune cell development and is vulnerable to influenza.
  • Additionally, the creation of NPG mice, which lack all lymphocyte types, allows for the successful engraftment of human tumor cell lines, enhancing the study of cancer and immunodeficiency models.
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The bone marrow (BM) stromal cell antigen-2 (BST-2), also known as tetherin, CD317, PDCA-1, or HM1.24, is a membrane protein overexpressed in several types of tumors and may act as a promising target for cancer treatment via antibody-dependent cellular cytotoxicity. BST-2 is also expressed in human BM stromal cells (BMSC), which support B cell development.

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Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by type 2 immune responses. Interleukin-25 (IL-25) is produced predominantly by epithelial cells. It can activate Th2 cells to produce type 2 cytokines such as IL-4, IL-5 and IL-13, contributing to host defense against nematodes.

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Exposure to various antigens derived from house dust mites (HDM) is considered to be a risk factor for development of certain allergic diseases such as atopic asthma, atopic dermatitis, rhinitis and conjunctivitis. Chitin is an insoluble polysaccharide (β-(1-4)-poly-N-acetyl-D-glucosamine) and a major component in the outer shell of HDMs. Mice exposed to chitin develop asthma-like airway eosinophilia.

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IL-25, a member of the IL-17 family of cytokines, is known to enhance type 2 immune responses, but suppress type 3 (IL-17A)-mediated immune responses. Mice deficient in IL-1 receptor antagonist (Il1rn mice) have excessive IL-1 signaling, resulting in spontaneous development of IL-1-, TNF- and IL-17A-dependent aortitis. We found that expression of II25 mRNA was increased in the aortae of Il1rn mice, suggesting that IL-25 may suppress development of IL-1-, TNF- and IL-17A-dependent aortitis in Il1rn mice by inhibiting type 3-mediated immune responses.

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Because cardiomyocyte generation is limited, the turnover of cardiomyocytes in adult heart tissues is much debated. We report here that cardiac pacemaker cells can generate cardiomyocytes from fibroblasts in vitro. Sinoatrial node cells (SANCs) were isolated from adult guinea pig hearts and were cultured at relatively low cell densities.

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  • Certain proteases from house dust mites and plants can trigger allergic airway inflammation by breaking down tight junctions between epithelial cells, resulting in airway eosinophilia in mice.
  • This study shows that inhalation of Aspergillus-derived proteases leads to airway eosinophilia through protease-activated receptor-2 (PAR2), highlighting their role over other cell receptors.
  • The eosinophilia is primarily mediated by innate immune cells rather than T, B, or NKT cells, with IL-33 being crucial for this response.
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IL-17C, which is a member of the IL-17 family of cytokines, is preferentially produced by epithelial cells in the lung, skin and colon, suggesting that IL-17C may be involved in not only host defense but also inflammatory diseases in those tissues. In support of that, IL-17C was demonstrated to contribute to development of T cell-dependent imiquimod-induced psoriatic dermatitis and T cell-independent dextran sodium sulfate-induced acute colitis using mice deficient in IL-17C and/or IL-17RE, which is a component of the receptor for IL-17C. However, the roles of IL-17C in other inflammatory diseases remain poorly understood.

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Levels of IL36α are known to be increased in specimens from patients with atopic dermatitis and psoriasis. In addition, it has been reported that IL-36α is crucial for development of imiquimod-induced psoriatic dermatitis in mice. On the other hand, the role of IL-36α in induction of allergic contact dermatitis/contact hypersensitivity (ACD/CHS) is poorly understood.

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IL-31, which is a member of the IL-6 family of cytokines, is produced mainly by activated CD4 T cells, in particular activated Th2 cells, suggesting a contribution to development of type-2 immune responses. IL-31 was reported to be increased in specimens from patients with atopic dermatitis, and IL-31-transgenic mice develop atopic dermatitis-like skin inflammation, which is involved in the pathogenesis of atopic dermatitis. However, the role of IL-31 in development of contact dermatitis/contact hypersensitivity (CHS), which is mediated by hapten-specific T cells, including Th2 cells, is not fully understood.

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Background: In addition to thymic stromal lymphopoietin and IL-33, IL-25 is known to induce T2 cytokine production by various cell types, including T2 cells, T9 cells, invariant natural killer T cells, and group 2 innate lymphoid cells, involved in T2-type immune responses. Because both T2-type and T17-type cells/cytokines are crucial for contact hypersensitivity (CHS), IL-25 can contribute to this by enhancing T2-type immune responses. However, the precise role of IL-25 in the pathogenesis of fluorescein isothiocyanate-induced CHS is poorly understood.

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Interleukin (IL)-25, which is a member of the IL-17 family of cytokines, induces production of such Th2 cytokines as IL-4, IL-5, IL-9 and/or IL-13 by various types of cells, including Th2 cells, Th9 cells and group 2 innate lymphoid cells (ILC2). On the other hand, IL-25 can suppress Th1- and Th17-associated immune responses by enhancing Th2-type immune responses. Supporting this, IL-25 is known to suppress development of experimental autoimmune encephalitis, which is an IL-17-mediated autoimmune disease in mice.

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  • TSLP promotes Th2 cytokine production, which plays a significant role in Th2-type immune responses and allergic disorders.
  • Research showed that house dust mite (HDM) extract triggers TSLP production in nasal epithelial cells, hinting at its role in allergic rhinitis.
  • Experiments with TSLP receptor-deficient mice indicated that the receptor is not essential for developing HDM-induced allergic rhinitis, as both normal and receptor-deficient mice reacted similarly to HDM exposure.
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Background: T cell immunoglobulin domain and mucin domain-containing molecule 3 (TIM-3), which is preferentially expressed on Th1 cells rather than Th2 cells, is considered to be a negative regulator of Th1 cell function. This suggests that TIM-3 indirectly enhances Th2-type immune responses by suppressing Th1 cell function.

Methods: To investigate TIM-3's possible involvement in Th2-type acute and chronic airway inflammation, wild-type and TIM-3-deficient (TIM-3) mice were sensitized and challenged with a house dust mite (HDM) extract.

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IL-25, IL-33 and TSLP, which are produced predominantly by epithelial cells, can induce production of Th2-type cytokines such as IL-4, IL-5 and/or IL-13 by various types of cells, suggesting their involvement in induction of Th2-type cytokine-associated immune responses. It is known that Th2-type cytokines contribute to host defense against malaria parasite infection in mice. However, the roles of IL-25, IL-33 and TSLP in malaria parasite infection remain unclear.

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House dust mite-derived proteases contribute to allergic disorders in part by disrupting epithelial barrier function. Interleukin-33 (IL-33), produced by lung cells after exposure to protease allergens, can induce innate-type airway eosinophilia by activating natural helper (NH) cells, a member of group 2 innate lymphoid cells (ILC2), to secrete Th2 type-cytokines. Because IL-33 also can induce mast cells (MCs) to secrete Th2 type-cytokines, MCs are thought to cooperate with NH cells in enhancing protease or IL-33-mediated innate-type airway eosinophilia.

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Background: Lower tube voltage has advantages for CT angiography, such as improved contrast

Objective: To evaluate the image quality of low-voltage (70 kV) CT for congenital heart disease and the ability of sinogram-affirmed iterative reconstruction to improve image quality.

Materials And Methods: Forty-six children with congenital heart disease (median age: 109 days) were examined using dual-source CT. Scans were performed at 80 kV and 70 kV in 21 and 25 children, respectively.

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Background: Viral infection is one of the risk factors for asthma exacerbation. However, which pathogens are related to asthma exacerbation in adults remains unclear.

Objective: The relation between various infections and adult asthma exacerbations was investigated in clinical practice.

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IL-17RA is a shared receptor subunit for several cytokines of the IL-17 family, including IL-17A, IL-17C, IL-17E (also called IL-25) and IL-17F. It has been shown that mice deficient in IL-17RA are more susceptible to sepsis than wild-type mice, suggesting that IL-17RA is important for host defense against sepsis. However, it is unclear which ligands for IL-17RA, such as IL-17A, IL-17C, IL-17E/IL-25 and/or IL-17F, are involved in the pathogenesis of sepsis.

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Epidemiological studies suggest an association between breakfast skipping and body weight gain, insulin resistance or type 2 diabetes. Time when meal is consumed affects postprandial increase in energy expenditure and blood glucose, and breakfast skipping may reduce 24 h energy expenditure and elevate blood glucose level. The present study evaluated the effect of breakfast skipping on diurnal variation of energy metabolism and blood glucose.

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Both interleukin (IL)-33 and IL-25 induce Th2 cytokine production by various cell types, suggesting that they contribute to development of allergic disorders. However, the precise roles of IL-33 and IL-25 in house dust mite (HDM)-induced allergic rhinitis (AR) remain unclear. Both IL-33 and IL-25 were produced mainly by nasal epithelial cells during HDM-induced AR.

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Heavy metals induce transcription of a number of mammalian genes, but in most cases the mechanism of induction has not been well characterized. The human heat shock protein 70 gene (hsp70) is activated by several heavy metals such as Cd and Zn, and the heat shock element (HSE) has been proposed to mediate metal response by previous studies. However, it was observed that the lack of further upstream sequences rendered the hsp70 promoter unresponsive to metals.

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Objective: Fat oxidation during exercise depends on nutritional state, and exercise performed in the post-absorptive state oxidizes more fat than that performed in the postprandial state. However, the effects of exercise on energy metabolism continue during the post-exercise period, and the difference in fat oxidation during exercise may be compensated for during the post-exercise period. The present study compared the effects of an acute exercise bout in the post-absorptive or postprandial state on 24 h fat oxidation.

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Purpose: The maximum limit of MR scanner noise and necessity of ear protection is defined in the IEC standard (IEC60601-2-33) of MR safety. With improvements in MR scanner performance, pulse sequences generating higher scanning noise have been used clinically. In this study, we investigated the factors significantly related to potential acoustic trauma cases (PATC) after MR examinations.

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