• YAKHAK HOEJI
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• v.36 no.4
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• pp.291-302
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• 1992

Effects of Zinc chloride on the immune responses were studied in ICR mice. ICR male mice were divided into 5 groups(10 mice/group) and Zinc chloride at doses of 0.3, 1.2, 4.8 and 19.2 mg/kg were orally administered to ICR male mice once a day for three weeks. Mice were sensitized and challenged with sheep red blood cells(S-RBC). The results of this study were summarized as follows; (1) Zinc chloride significantly increased the body weight rate, the weight ratios of spleen and thymus to body weight and the number of circulating leukocyte, but significantly decreased them at the high dose of it, and increased dose-dependently the weight ratio of liver to body weight. (2) Zinc chloride significantly increased hemagglutination titer, Arthus reaction and plaque forming cell related to humoral immunity, but significantly decreased them at the high dose of it. (3) Zinc chloride significantly increased delayed-type hypersensitivity reaction and rosette forming cell related to cellular immunity, but significantly decreased them at the high dose of it. (4) Zinc choride significantly enhanced phagocytic activity, but significantly decreased according to the increase of its dose. These results suggest that high dose of zinc chloride decreased humoral, cellular and non-specific immune responses.

• Journal of Animal Science and Technology
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• v.65 no.4
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• pp.804-817
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• 2023

This study was conducted to evaluate the effects of co-dried fish protein hydrolysate (CFPH) on broilers performance, intestinal microbiology, and cellular immune responses. Five hundred one-day-old (Ross 308) male broilers were allocated to four treatments with five replicates of 25 birds in a completely randomized design. The experimental treatments included four levels of CFPH (0% as the control, 2.5%, 5%, and 7.5%) in the isonitrogenous and isocaloric diets. During the experiment, body weight (BW) and feed intake (FI) were periodically recorded in addition to calculating average daily gain (ADG), feed conversion ratio (FCR), liveability index, and European broiler index (EBI). In addition, cellular immune responses were evaluated at 30 days of age. On day 42, ileal contents were obtained to examine the microbial population. Based on the findings, Dietary supplementation of 5 and 7.5% CFPH increased the percentage of the thigh while decreasing the relative weight of the gizzard compared to the control group. The highest relative length of jejunum was observed in birds receiving 2.5 and 5% CFPH, and its highest relative weight belonged to birds fed with 5% CFPH. The number of coliforms, enterobacters, and total gram-negative bacteria in the intestines of birds receiving CFPH was less than that of the control group. In general, the application of CFPH in broiler nutrition can decrease the level of soybean meal in diet and it can be considered as a new protein supplement in poultry production. It is suggested to study the incorporation of this new supplement in other livestock's diets.

• BMB Reports
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• v.53 no.7
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• pp.385-390
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• 2020

Inflammatory Bowel Disease is caused by an acute or chronic dysfunction of the mucosal inflammatory system in the intestinal tract. In line with the results of our previous study, wherein we found that the PKCα-LSD1-NF-κB signaling plays a critical role in the prolonged activation of the inflammatory response, we aimed to investigate the effect of signaling on colitis in the present study. Lsd1 S112A knock-in (Lsd1^SA/SA) mice, harboring a deficiency in phosphorylation by PKCα, exhibited less severe colitis symptoms and a relatively intact colonic epithelial lining in dextran sulfate sodium (DSS)-induced colitis models. Additionally, a reduction in pro-inflammatory gene expression and immune cell recruitment into damaged colon tissues in Lsd1^SA/SA mice was observed upon DSS administration. Furthermore, LSD1 inhibition alleviated colitis symptoms and reduced colonic inflammatory responses. Both LSD1 phosphorylation and its activity jointly play a role in the progression of DSS-induced colitis. Therefore, the inhibition of LSD1 activity could potentially protect against the colonic inflammatory response.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.5
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• pp.707-714
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• 2008

The experiment was conducted to evaluate the effect of ${\beta}$-1,3/1,6-glucan on growth performance, immunity and endocrine responses of weanling piglets. One hundred and eighty weanling piglets (Landrace$\times$Large White, $7.20{\pm}0.25kg$ BW and $28{\pm}2$ d of age) were randomly fed 1 of 5 treatment diets containing dietary ${\beta}$-1,3/1,6-glucan supplemented at 0, 25, 50, 100 and 200 mg/kg for 4 wks. Each treatment was replicated in 6 pens containing 6 pigs per pen. On d 14 and 28, body weight gain, feed consumption and feed efficiency were recorded as measures of growth performance. Peripheral blood lymphocyte proliferation and serum immunoglobulin G (IgG) were measured to study the effect of dietary ${\beta}$-1,3/1,6-glucan supplementation on immune function. Plasma prostaglandin E2 (PGE2), growth hormone (GH) and ghrelin were measured to investigate endocrine response to ${\beta}$-1,3/1,6-glucan supplementation. Our results suggest that average daily gain (ADG) and feed efficiency had a quadratic increase trend with dietary ${\beta}$-1,3/1,6-glucan supplementation from d 14 to 28, whereas it had no significant effect on average daily feed intake (ADFI). The treatment group fed with 50 mg/kg dietary ${\beta}$-1,3/1,6-glucan supplementation showed a numerical increase in ghrelin, a similar change trend with ADG and no significant effect on GH. Lymphocyte proliferation indices, serum IgG and plasma PGE2 concentrations varied linearly with dietary supplementation levels of ${\beta}$-1,3/1,6-glucan on d 14. Higher levels of ${\beta}$-1,3/1,6-glucan may have a transient immuno-enhancing effect on the cellular and humoral immune function of weanling piglets via decreased PGE2. Taking into account both immune response and growth performance, the most suitable dietary supplementation level of ${\beta}$-1,3/1,6-glucan is 50 mg/kg for weanling piglets.

• Korean Journal of Pharmacognosy
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• v.27 no.3
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• pp.274-281
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• 1996

Ulmus parvifolia has been used as a traditional folk medicine to treat the carbuncle in deep skin. In this study, the effect of water extract of root bark of Ulmus parvifolia (WUP) on the carbuncle, pain, inflammation and hypersensitivity was evaluated in animal models. The administration of WUP significantly decreased the size of Staphylococcus aureus ($10^8$ cells/mouse)-induced carbuncle, and also exhibited analgesic activity in the HAc-induced writhing syndrome at doses of 50-500 mg/kg. It also showed significant anti-inflammatory activity in the carageenin- and complete Freund's adjuvant-induced inflammation. In the histamine-induced anaphylaxis, it decreased the percent of mortality by protecting mice treated with Bordetella pertussis. In the immune responses in the mice sensitized and challenged with sheep red blood cells, the Arthus reaction determined by swelling of foot pad at 4 h after challenge, HA titer, HY titer and PFC which can be used to evaluate the humoral immune response were significantly suppressed by oral administration of WUP at doses of 100 and 200mg/kg. The cellular immune responses in the same mice such as delayed type hypersensitivity determined by swelling of foot pad at 24 h after challenge and RFC were also significantly suppressed in the same manner.

• Molecules and Cells
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• v.42 no.1
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• pp.1-7
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• 2019

Macrophage is an important innate immune cell that not only initiates inflammatory responses, but also functions in tissue repair and anti-inflammatory responses. Regulating macrophage activity is thus critical to maintain immune homeostasis. Tyro3, Axl, and Mer are integral membrane proteins that constitute TAM family of receptor tyrosine kinases (RTKs). Growing evidence indicates that TAM family receptors play an important role in anti-inflammatory responses through modulating the function of macrophages. First, macrophages can recognize apoptotic bodies through interaction between TAM family receptors expressed on macrophages and their ligands attached to apoptotic bodies. Without TAM signaling, macrophages cannot clear up apoptotic cells, leading to broad inflammation due to over-activation of immune cells. Second, TAM signaling can prevent chronic activation of macrophages by attenuating inflammatory pathways through particular pattern recognition receptors and cytokine receptors. Third, TAM signaling can induce autophagy which is an important mechanism to inhibit NLRP3 inflammasome activation in macrophages. Fourth, TAM signaling can inhibit polarization of M1 macrophages. In this review, we will focus on mechanisms involved in how TAM family of RTKs can modulate function of macrophage associated with anti-inflammatory responses described above. We will also discuss several human diseases related to TAM signaling and potential therapeutic strategies of targeting TAM signaling.

• Korean Journal of Veterinary Research
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• v.36 no.4
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• pp.839-844
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• 1996

This study was designed to investigated the effects of cadmium(Cd) feeding on the humoral immune responses such as PFC-responses and production of immunoglobulins in BALB/c mice. The results obtained were summarized as follows; 1. Total PFCs of direct IgM antibody response were significantly decreased in all Cd-fed goups, whereas total PFCs of IgG antibody response were slightly increased. 2. In secondary immunization, total HA titers were increased in all Cd groups as compared with control, especially in 100ppmm group and also IgG titers were slightly increased except for 50ppm group. 3. The levels of $IgG_1$ were increased to 5.5% 18.7%, 17.4% and 7.2% in 25, 50, 100 and 200ppm groups as compared with control, respectively. And also the levels of IgE were increased to 5.7%, 7.3%, 8.7% and 0.4% in those of Cd groups, in order. Conclusively, concentrations of $IgG_1$, and IgE were increased in all Cd groups. Based on the results of this study and previous report, it was shown that Cd might affect humoral immune responses by modifying the distribution and function of cells playing in the cellular immune response.

• Food Science of Animal Resources
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• v.42 no.5
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• pp.903-914
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• 2022

Probiotics are currently considered as one of tools to modulate immune responses under specific clinical conditions. The purpose of this study was to evaluate whether oral administration of three different probiotics (Lactiplantibacillus plantarum CJLP243, CJW55-10, and CJLP475) could evoke a cell-mediated immunity in immunodeficient mice. Before conducting in vivo experiments, we examined the in vitro potency of these probiotics for macrophage activation. After co-culture with these probiotics, bone marrow derived macrophages (BMDMs) produced significant amounts of proinflammatory cytokines including interleukin-6 (IL-6), IL-12, and tumor necrosis factor-α (TNF-α). Levels of inducible nitric oxide synthase (inos) and co-stimulatory molecules (CD80 and CD86) were also upregulated in BMDMs after treatment with some of these probiotics. To establish an immunocompromised animal model, we intraperitoneally injected mice with cyclophosphamide on day 0 and again on day 2. Starting day 3, we orally administered probiotics every day for the last 15 d. After sacrificing experimental mice on day 18, splenocytes were isolated and co-cultured with these probiotics for 3 d to measure levels of several cytokines and immune cell proliferation. Results clearly indicated that the consumption of all three probiotic strains promoted secretion of interferon-γ (IFN-γ), IL-1β, IL-6, IL-12, and TNF-α. NK cell cytotoxicity and proliferation of immune cells were also increased. Taken together, our data strongly suggest that consumption of some probiotics might induce cell-mediated immune responses in immunocompromised mice.

• The Plant Pathology Journal
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• v.40 no.3
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• pp.235-250
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• 2024

During the infection process, plant pathogenic fungi encounter plant-derived oxidative stress, and an appropriate response to this stress is crucial to their survival and establishment of the disease. Plant pathogenic fungi have evolved several mechanisms to eliminate oxidants from the external environment and maintain cellular redox homeostasis. When oxidative stress is perceived, various signaling transduction pathways are triggered and activate the downstream genes responsible for the oxidative stress response. Despite extensive research on antioxidant systems and their regulatory mechanisms in plant pathogenic fungi, the specific functions of individual antioxidants and their impacts on pathogenicity have not recently been systematically summarized. Therefore, our objective is to consolidate previous research on the antioxidant systems of plant pathogenic fungi. In this review, we explore the plant immune responses during fungal infection, with a focus on the generation and function of reactive oxygen species. Furthermore, we delve into the three antioxidant systems, summarizing their functions and regulatory mechanisms involved in oxidative stress response. This comprehensive review provides an integrated overview of the antioxidant mechanisms within plant pathogenic fungi, revealing how the oxidative stress response contributes to their pathogenicity.

• Molecules and Cells
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• v.28 no.3
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• pp.139-148
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• 2009

Cell death has been traditionally classified in apoptosis and necrosis. Apoptosis, known as programmed cell death, is an active form of cell death mechanism that is tightly regulated by multiple cellular signaling pathways and requires ATP for its appropriate process. Apoptotic death plays essential roles for successful development and maintenance of normal cellular homeostasis in mammalian. In contrast to apoptosis, necrosis is classically considered as a passive cell death process that occurs rather by accident in disastrous conditions, is not required for energy and eventually induces inflammation. Regardless of different characteristics between apoptosis and necrosis, it has been well defined that both are responsible for a wide range of human diseases. Glycogen storage disease type I (GSD-I) is a kind of human genetic disorders and is caused by the deficiency of a microsomal protein, glucose-6-phosphatase-${\alpha}$ ($G6Pase-{\alpha}$) or glucose-6-phosphate transporter (G6PT) responsible for glucose homeostasis, leading to GSD-Ia or GSD-Ib, respectively. This review summarizes cell deaths in GSD-I and mostly focuses on current knowledge of the neutrophil apoptosis in GSD-Ib based upon ER stress and redox signaling.