• Journal of Preventive Medicine and Public Health
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• v.27 no.1 s.45
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• pp.11-24
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• 1994

The studies reported here were undertaken to investigate the effects of mercury chloride on immune system of Balb/c mouse employing a flexible tier of in vitro and in vivo assays. Mercury chloride inhibited the proliferative responses of spleen cells to lipopolysaccharide, pokeweed mitogen, and phytohemagglutinin as a dose-dependent manner. This inhibitory effect was observed not only when $HgCl_2$ was added 2nd or 3rd day of 3 days culture period but also when spleen cells was pretreated with $HgCl_2$ for 2 hours. Mercury chloride, however, potentiated the production of IgM and IgG from spleen cells. During the $HgCl_2$ administration by drinking for 3 weeks, the weight gain of mice was significantly blunted than that o control group mice, while no overt signs related to mercury toxicity were noted in any mice of experimental group. There was no change in thymus and spleen weights, and in histological findings of kidney, bone marrow of femur, thymus, spleen, and popliteal lymph node after 3 weeks of mercury exposure. However, $HgCl_2$ induced a significant increase of total serum IgM, IgG including $IgG_1,\;IgG_{2a}\;and\;IgG_{2b}$, and IgE in Balb/c mice. Treatment in vivo with anti-IL-4 monoclonal antibody significantly abrogated the $HgCl_2$-induced increase in total serum IgG1 and IgE. Whereas $HgCl_2$ potentiated total serum IgM and IgG, there was no difference in total serum hemagglutinin to SRBC (Sheep Red Blood Cell) between experimental and control group mice when these mice were immunized with SRBC. All these findings observed in Balb/c mice suggest that mercury perturbates well-orchestrated regulation of immune responses before developing histopathological changes in lymphoid tissues.

• Journal of Sasang Constitutional Medicine
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• v.12 no.1
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• pp.201-215
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• 2000

1. Background and Purpose According to Sasang constitutional medicine, Yuldahansotang(YHT) is a useful prescription for Teaumin patients with a variety of neurologic disorders. Then, I investigated about certain relationships between the effect of YHT and the changes of immune system, especially cytokine network. 2. Methods We studied 8 Taeumin patients with Cerbral infarction. They were treated with YHT in constitutional clinic of Wonkwang Kwagnju Oriental Hospital. We investigated the changes of cytokine network of them. We also investigated cytokine release by lipopolysaccharide- activated peripheral blood mononuclear cells from healthy Taeumin controls. 3. Results The mean interleukin (IL)-2 plasma levels were slightly lower in the plasma of patients than in normal group, whereas the mean IL-4, IL-6 and IgE levels were significantly higher. But there were no significant differences in $interferon-{\gamma}$($IFN-{\gamma}$) levels between each group. After administration of YHT for two to four weeks, plasma levels of $IFN-{\gamma}$ and IL-2 derived from T helper (Th) 1 cells were elevated significantly, whereas plasma levels of IL-4 and IL-6 derived from Th2 cells were reduced significantly. Plasma levels of IgE were reduced significantly, too. During the period of YHT administration, other adverse effects are not shown. It is increased significantly to Cytokine release by lipopolysaccharide -activated peripheral blood mononuclear cells from healthy Taeumin controls. And the release of $IFN-{\gamma}$, IL-2 and IL-6 was progressively decreased in the plasma treated with YHT. It shows regulatory effects of YHT to cytokine production.

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.2
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• pp.180-185
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• 1999

Effects of host immunization on bacterial translocation and growth performance in weanling piglets were studied. Twenty four barrows were assigned to one of two immunization treatments: Control group (CON: immunized with placebo) or Immunization group [IMMU: immunized with Antigen cocktail; Keyhole limpet hemocyanin (KLH), Ovalbumin (OA), and Tetanus toxoid (TT)]. On d0, piglets were weaned and intramuscularly immunized with 2 ml of placebo or Antigen cocktail, respectively. Antigen-specific Ig titers were determined by ELISA (Enzyme Linked ImmunoSorbent Assay). Ig titers to E. coli-derived lipopolysaccharides (LPS) were measured as the indicator of bacterial translocation. Ig titers to LPS were higher (p<0.10, 0.05 or 0.01) in CON group before immunization (d0), but the difference disappeared with time and IgA titers to LPS became higher (p<0.05) in IMMU group on d39. In IMMU group, IgG titers to LPS from d28 onwards showed positive correlations (p<0.10, 0.05, 0.01 or 0.001) with IgG titers to KLH from d11 onwards and with IgM titers to KLH from d7 onwards. Generally, growth performance was negatively related to IgG titers to LPS. Average daily gain for d28 to d35 showed negative correlations (p<0.10, 0.05, or 0.01) with IgG titers to LPS on d28 onwards in immunization group. These results reveal some evidences that host immunization might facilitate bacterial translocation and high humoral immune responses to LPS are negatively related with the growth performance.

• Tuberculosis and Respiratory Diseases
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• v.78 no.3
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• pp.218-226
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• 2015

Background: Eph receptors and ephrin ligands have several functions including angiogenesis, cell migration, axon guidance, fluid homeostasis, oncogenesis, inflammation and injury repair. The EphA2 receptor potentially mediates the regulation of vascular permeability and inflammation in response to lung injury. Methods: Mice were divided into 3 experimental groups to study the role of EphA2 signaling in the lipopolysaccharide (LPS)-induced lung injury model i.e., IgG+phosphate-buffered saline (PBS) group (IgG instillation before PBS exposure), IgG+LPS group (IgG instillation before LPS exposure) and EphA2 monoclonal antibody (mAb)+LPS group (EphA2 mAb pretreatment before LPS exposure). Results: EphA2 and ephrinA1 were upregulated in LPS-induced lung injury. The lung injury score of the EphA2 mAb+LPS group was lower than that of the IgG+LPS group ($4.30{\pm}2.93$ vs. $11.45{\pm}1.20$, respectively; p=0.004). Cell counts (EphA2 mAb+LPS: $11.33{\times}10^4{\pm}8.84{\times}10^4$ vs. IgG+LPS: $208.0{\times}10^4{\pm}122.6{\times}10^4$; p=0.018) and total protein concentrations (EphA2 mAb+LPS: $0.52{\pm}0.41mg/mL$ vs. IgG+LPS: $1.38{\pm}1.08mg/mL$; p=0.192) were decreased in EphA2 mAb+LPS group, as compared to the IgG+LPS group. In addition, EphA2 antagonism reduced the expression of phospho-p85, phosphoinositide 3-kinase $110{\gamma}$, phospho-Akt, nuclear factor ${\kappa}B$, and proinflammatory cytokines. Conclusion: This results of the study indicated a role for EphA2-ephrinA1 signaling in the pathogenesis of LPS-induced lung injury. Furthermore, EphA2 antagonism inhibits the phosphoinositide 3-kinase-Akt pathway and attenuates inflammation.

• Asian-Australasian Journal of Animal Sciences
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• v.19 no.11
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• pp.1665-1670
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• 2006

The objective of this research was to provide the characterization and method for producing anti-E. coli O157:H7 antibodies in egg-laying hens and to determine if the antibody can restrain the proliferation of E. coli O157:H7 in-vitro. Selected antigenic fractions (whole cell, outer membrane protein and lipopolysaccharide (LPS)) from E. coli O157:H7 were injected to hens in order to produce anti-E. coli O157:H7 antibodies. The immune response and the egg yolk antibodies of laying hens against the whole cell, outer membrane protein and LPS antigens were monitored by ELISA. The level of antibodies against whole cell antigen monitored through ELISA sharply increased after the initial immunization, and it was found to be maximum on day 49 however, the level was maintained up to day 70. Antibodies (5 mg/ml) directed against the whole cell inhibited E. coli proliferation 10-13 times more than outer membrane protein or LPS. The antibody response against the whole cell antigens appeared to have higher activity in restraining the proliferation of E. coli O157:H7 than antibody against outer membrane protein or LPS. Results reflected that increasing the IgY's in the egg yolk could prevent greater economic losses due to human and animal health from pathogenic bacteria i.e. E. coli O157:H7.

• Journal of Microbiology and Biotechnology
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• v.26 no.6
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• pp.1035-1045
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• 2016

To evaluate the effects of lactic acid bacteria (LAB) on Peyer's patch cells, mice were treated with a high dose of kanamycin to disturb the gut microbial environment. The overarching goal was to explore the potential of LAB for use as a dietary probiotic that buffers the negative consequences of antibiotic treatment. In vitro, LAB stimulated the production of immunoglobulin A (IgA) from isolated Peyer's patch cells. Inflammation-related genes (TNF-α, IL-1β, and IL-8) were up-regulated in Caco-2 cells stimulated with lipopolysaccharide (LPS), while tight-junction-related genes (ZO-1 and occludin) were down-regulated; the effects of LPS on inflammatory gene and tight-junction gene expression were reversed by treatment with LAB. Mice treated with a high dose of kanamycin showed increased serum IgE levels and decreases in serum IgA and fecal IgA levels; the number of Peyer's patch cells decreased with kanamycin treatment. However, subsequent LAB treatment was effective in reducing the serum IgE level and recovering the serum IgA and fecal IgA levels, as well as the number of Peyer's patch cells. In addition, ZO-1 and occludin mRNA levels were up-regulated in the ileum tissues of mice receiving LAB treatment. Lactic acid bacteria can enhance the intestinal immune system by improving the integrity of the intestinal barrier and increasing the production of IgA in Peyer's patches. Lactic acid bacteria should be considered a potential probiotic candidate for improving intestinal immunity, particularly in mitigating the negative consequences of antibiotic use.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.4
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• pp.379-389
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• 2018

A nucleobase adenine is a fundamental component of nucleic acids and adenine nucleotides. Various biological roles of adenine have been discovered. It is not produced from degradation of adenine nucleotides in mammals but produced mainly during polyamine synthesis by dividing cells. Anti-inflammatory roles of adenine have been supported in IgE-mediated allergic reactions, immunological functions of lymphocytes and dextran sodium sulfate-induced colitis. However adenine effects on Toll-like receptor 4 (TLR4)-mediated inflammation by lipopolysaccharide (LPS), a cell wall component of Gram negative bacteria, is not examined. Here we investigated anti-inflammatory roles of adenine in LPS-stimulated immune cells, including a macrophage cell line RAW264.7 and bone marrow derived mast cells (BMMCs) and peritoneal cells in mice. In RAW264.7 cells stimulated with LPS, adenine inhibited production of pro-inflammatory cytokines $TNF-{\alpha}$ and IL-6 and inflammatory lipid mediators, prostaglandin $E_2$ and leukotriene $B_4$. Adenine impeded signaling pathways eliciting production of these inflammatory mediators. It suppressed $I{\kappa}B$ phosphorylation, nuclear translocation of nuclear factor ${\kappa}B$ ($NF-{\kappa}B$), phosphorylation of Akt and mitogen activated protein kinases (MAPKs) JNK and ERK. Although adenine raised cellular AMP which could activate AMP-dependent protein kinase (AMPK), the enzyme activity was not enhanced. In BMMCs, adenine inhibited the LPS-induced production of $TNF-{\alpha}$, IL-6 and IL-13 and also hindered phosphorylation of $NF-{\kappa}B$ and Akt. In peritoneal cavity, adenine suppressed the LPS-induced production of $TNF-{\alpha}$ and IL-6 by peritoneal cells in mice. These results show that adenine attenuates the LPS-induced inflammatory reactions.

• Journal of Preventive Medicine and Public Health
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• v.28 no.1 s.49
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• pp.27-42
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• 1995

The in vivo and in vitro humoral and cell-mediated immune responses of lymphocytes of BALB/c mouse exposed to mercury chloride$(HgCl_2)$ were investigated. In vitro exposure of the splenocytes to mercury chloride produced overt cytotoxicity in 3 hours period. The $IC_{50}$(the concentration required to inhibit a splenocyte viability by 50%) for mercury chloride was >0.1mM for cytotoxicity. In vivo mercury chloride exposed mice were significantly depressed delayed type hypersensitivity(DTH) response to sheep red blood cells(SRBC) in a dose-dependent manner compared with control group. Mercury chloride inhibited the proliferative responses of splenocytes to lipopolysaccharide, pokeweed mitogen, concanavalin A and phytohemagglutinin in a dose-dependent manner. Hemagglutinin response to SRBC in mercury chloride exposed mice was significantly depressed in a dose-dependent manner compared with control group. After 7 weeks of mercury chloride exposure in vivo, mercury chloride induced an increase of nonspecific serum $IgG_1$ and IgE levels in BALB/c mice.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.28 no.1
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• pp.23-31
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• 2015

Objectives : Allergic disease has been well known as an IgE-dependent immunologic response. Recently, interest about the late inflammatory reaction has grown up as well as early allergic reaction characterized by IgE and mast cell. The purpose of this study was to find the anti-inflammatory effect of Gamiyunjo-tang(GMYJT) in allergic reaction. Methods : The experiment was performed using Raw 264.7 cells pretreated with GMYJT extracts. In this study, we observed the toxicity of cells by MTT analysis and measured the production of LPS-induced NO, $PGE_2$, IL-$1{\beta}$, IL-6 and TNF-${\alpha}$ at a concentration of 50, 100, 200 and $400{\mu}g/ml$. Results : No toxicity of GMYJT (50, 100, 200, $400{\mu}g/ml$) on RAW 264.7 cells was found after 24 hours incubation. LPS-induced NO production was reduced after treatment with GMYJT (100, 200, $400{\mu}g/ml$)(P<0.05). $PGE_2$ was reduced after treatment with GMYJT (100, 200, $400{\mu}g/ml$)(P<0.05). IL-$1{\beta}$ did not decrease at any dose. IL-6 decreased at 200, $400{\mu}g/ml$(P<0.05). TNF-${\alpha}$ production decreased only at $400{\mu}g/ml$(P<0.05). Conclusions : These data suggest that GMYJT has anti-inflammatory effects in late allergic reaction.

• Natural Product Sciences
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• v.12 no.2
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• pp.67-73
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• 2006

Antiallergic activities of two variants of Artemisia princeps Pampanini SJ-1 (named as Sajabalssuk) and SS-1 (named as Sajuarissuk) cultivated in Ganghwado, which contain high content of eupatilin compared to those cultured by other places, were investigated to evaluate the possibility as inhibitors against allergic diseases. Ethanol and supercritical fluid extracts of SJ-1 and SS-1 inhibited the release of ${\beta}-hexosaminidase$ from RBL-2H3 cells, although their water extracts were inactive. These extracts potently inhibited lipopolysaccharide-induced NO production of RAW264.7. However, these extracts almost did not scavenge free radicals. Oral administration of these extracts to mice inhibited passive cutaneous anaphylaxis reaction induced by IgE, and acute dermatitis induced by 12-O-tetradecanoylphorbol-13-acetate. However, these extracts did not inhibit chronic dermatitis. Scratching behaviors, vascular permeability, and writhing syndromes were weakly inhibited by these extract at a dose of 50 mg/kg. Based on these findings, we believe that SJ-1 and SS-1 can improve IgE-induced allergic diseases such as rhinitis and asthma.