• Nutritional Sciences
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• v.1 no.1
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• pp.22-28
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• 1998

Plasma concentrations of Vitamins E and A were measured in 15 non-insulin dependent Korean female subjects and 15 age-matched normal subjects using reversed-phase high-performance liquid chromatography. No differences were found in plasma Vitamin E concentrations between the 2 groups. Plasma Vitamin A concentrations were higher in subjects with non-insulin dependent diabetes melitus (NIDDM). The effects were evaluated of 4 weeks of daily supplementation of 400 mg Vitamin E on plasma levels of these two vitamins. In addition, the effects were observed for Vitamin E supplementation on oxidative stress and immune-related compound productions in non-insulin dependent diabetic patients and control subjects. After treatment with Vitamin E, plasma Vitamin E concentrations were significantly elevated in both groups. Basal plasma thiobarbituric acid reactive substances (TBABS) were identical, and a decreased level of TBARS caused by Vitamin E was observed only in the diabetic group (0.02739$\pm$0.0024 versus 0.01814$\pm$0.0008 nmols malondialdehyde equivalents/dl plasma ; p<0.05). The basal and after-treatment levels of immunoglobulins A, G, M were identical in control and diabetic groups, indicating that Vitamin E did not appear to alter gross humoral responses in this study. However, elevation of Complement 3 ($C_3$) was noticed due to Vitamin E supplementation, revealing a possible effect of vitamin E on one aspect of humoral immunity, Furthermore, an increase in prostaglandin E_2 ($PGE_2$) levels in diabetic patients was normalized by Vitamin E supplementation. This suggests indirectly that the depressed cell-mediated response due to elevated $PGE_2$ could be normalized. For the definitive antioxidant intake recommendations for prevention and treatment of adverse effects of non-insulin dependent diabetes, evidence from intervention trials like this study should be collected. The present data suggests that Vitamin E may oxen some protective effects against oxidative damage and might have beneficial effects of partial immune-stimulation.

• Tuberculosis and Respiratory Diseases
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• v.47 no.1
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• pp.13-25
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• 1999

Background: Ineffective cell-mediated immune response in human tuberculosis is associated with a depressed Thl cytokine response and reduced production of IFN-$\gamma$. Most persons infected with Mycobacterium tuberculosis are healthy tuberculin reactors with protective immunity, but a minority with ineffective immunity develop extensive pulmonary tuberculosis. The cell-mediated immune response is an important aspect of host resistance to mycobacterial infection and is believed to be tightly regulated by a balance between Th1 cytokines including IFN-$\gamma$, IL-12, IL-18, regulated on activation, normal T cell expressed and secreted (RANTES) and Th2 counterparts such as IL-4, monocyte chemoattractant protein-l (MCP-l). Methods: Proliferation and mRNA expression of IFN-$\gamma$, RANTES and MCP-l by RT-PCR in peripheral blood mononuclear cells (PBMCs) in response to in vitro stimulation with mycobacterial antigens were compared in pulmonary tuberculosis patients with cured and treatment failure and in tuberculin-positive and tuberculin-negative healthy subjects. Results: Defective proliferative responsiveness to aqueous TSP antigen was involved with treatment failure tuberculosis patients. Aqueous TSP antigen-induced IFN-$\gamma$ and RANTES mRNA expression was decreased in treatment failure tuberculosis patients compared with healthy tuberculin reactors and cured tuberculosis patients (23.1 % versus 90.0% for IFN-$\gamma$ and 46.2% versus 70.0% versus 46.2% for RANTES). The frequency of MCP-l mRNA expression to aqueous TSP antigen in treatment failure tuberculosis patients was greater than in healthy tuberculin reactors and cured tuberculosis patients (76.9% versus 40.0%). Conclusion: The increasing expression of MCP-1 mRNA in response to aqueous TSP antigen might be predicted to favor Th1 responses and restricted Th1 responses in treatment failure of pulmonary tuberculosis.

• Journal of Ginseng Research
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• v.45 no.3
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• pp.456-463
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• 2021

Background: Keratinocytes form a physical barrier and act as an innate immune cell in skin. Keratinocytes secrete pro-inflammatory cytokines, such as interleukin (IL)-1β, resulting from inflammasome activation when exposed to ultraviolet (UV) irradiation. Korean Red Ginseng extracts (RGE) have been well-studied as modulators of inflammasome activation in immune cells, such as macrophages. In the study, we elucidated the role of RGE on the UV-mediated inflammasome activation in keratinocytes compared with that in macrophages. Methods: Human skin keratinocyte cells (HaCaT), human epidermal keratinocytes (HEK), human monocyte-like cells (THP-1), and mouse macrophages were treated with RGE or a saponin fraction (SF) or non-saponin fraction (NS) of RGE before and after UV irradiation. The secretion levels of IL-1β, as an indicator of inflammasome activation, were analyzed. Results: The treatment of RGE or SF in macrophages after UV irradiation inhibited IL-1β secretion, but similar treatment in HaCaT cells did not. However, the treatment of RGE or SF in HaCaT cells in the presence of poly I:C, a toll-like receptor (TLR) 3 ligand, before UV exposure elicited the inhibition of the IL-1β secretion. The inhibition was caused by the disruption by RGE or SF of the TLR mediating up-regulation of the pro-IL-1β and NLRP3 genes during the priming step. Conclusion: RGE and its saponins inhibit IL-1β secretion in response to UV exposure in both keratinocytes and macrophages. In particular, RGE treatment interrupted only the priming step in keratinocytes, although it did attenuate both the priming and activation steps in macrophages.

• Journal of Life Science
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• v.24 no.2
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• pp.154-160
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• 2014

Ghost cells have been recognized as eliciting humoral and cell-mediated immune responses and have also been predicted to play a role as an immune adjuvant. In this study, we used the intramuscular (IM) route to inject BALB/c mice with four vaccine groups constructed from Salmonella typhimurium ghost (STG) cells originating from different virulent strains and complex STG groups instead of heat-labile toxin (LT)-B, a type of adjuvant. Although the complex STG groups exhibited a response after a short delay, the groups showed final total IgG levels similar to those of the LT-B group, which encodes LT-B from pMMP300. The IgG1 response to the ${\chi}$3339 group was the highest response at 6 weeks, whereas IgG2a responses to the ${\chi}$3339 and JOL389 groups were higher at 6 and 8 weeks compared to those of the LT-B group. The response of vaginal sIgA to the LT-B group was generally higher than that of the other groups, whereas fecal sIgA to the LT-B group exhibited lower responses. Protection to virulent S. typhimurium in all groups was above 80%, which was similar to the LT-B group. Taken together, we suggest that STG complex groups can be used as an immune adjuvant instead of LT-B.

• Korean Journal of Psychosomatic Medicine
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• v.7 no.2
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• pp.196-202
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• 1999

The purpose of the study was to determine the effect of vitamin B complex on stress-induced immune alteration. 21 medical students participated in the study 4 weeks before an academic examination period(baseline), 2 weeks before the exam period and during the exam period. Among them, 10 subjects were given vitamin B complex for 4 weeks, and 11 were not given vitamin B during the whole period. Cell-mediated immune function was measured by lymphocyte proliferative response to phytohemagglutinin(PHA) and interleukin-2(IL-2) production. Global assessment of recent stress(GARS) scale and symptom checklist-90-revised(SCL-90-R) were used to measure the level of subjective stress and psychopathology. Vitamin group had significantly lower scores of anxiety scale on SCL-90-R than non-vitamin group. No significant differences were found in lymphocyte proliferative response to PHA and IL-2 production between vitamin and non-vitamin groups during each period. There were no significant differences in change of of each of the two immune parameters over time as well as between vitamin and non-vitamin groups. However, lymphocyte proliferative response to PHA was significantly increased over time. In conclusion, it was suggested that vitamin B complex is likely to decrease anxiety level, and that exam stress might enhance lymphocyte proliferation regardless of vitamin B.

• Toxicological Research
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• v.34 no.1
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• pp.7-12
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• 2018

Laboratory animal models have been developed to investigate preventive or therapeutic effect of medicinal products, or occurrence or progression mechanism of atopic dermatitis (AD), a pruritic and persistent inflammatory skin disease. The murine model with immunologic phenomena resembling human AD was introduced, which demonstrated skewedness toward predominance of type-2 helper T cell reactivity and pathophysiological changes similar as human AD following 2,4-dinitrochlorobenzene (DNCB) sensitization and challenge. Molecular mechanism on the DNCB-mediated AD was further evaluated. Skin tissues were collected from mice treated with DNCB, and each tissue was equally divided into two sections; one for protein and the other for mRNA analysis. Expression of filaggrin, an important protein for keratinocyte integrity, was evaluated through SDS-PAGE. Level of mRNA expression for cytokines was determined through semi-quantitative reverse transcriptase polymerase chain reaction. Expression of filaggrin protein was significantly enhanced in the mice treated with DNCB compared with the vehicle (acetone : olive oil = 4 : 1 mixture) treatment group or the normal group without any treatment. Level of tumor necrosis factor-alpha and interleukin-18 mRNA expression, cytokines involved in activity of type-1 helper T ($T_H1$) cell, was significantly downregulated in the AD group compared with other control groups. These results suggest that suppression of $T_H1$ cell-mediated immune response could be reflected into the skin tissue of mice treated with DNCB for AD induction, and disturbance of keratinocyte integrity might evoke a compensatory mechanism.

• IMMUNE NETWORK
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• v.3 no.2
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• pp.136-144
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• 2003

Oral administration of antigen has long been considered as a promising alternative for the treatment of chronic autoimmune diseases including rheumatoid arthritis (RA), and oral application of type II collagen (CII) has been proven to improve pathogenic symptoms in RA patients without problematic side effects. To further current understandings about the immune suppression mechanisms mediated by orally administered antigens, we examined the changes in IgG subtypes, T-cell proliferative response, and proportion of interleukin (IL)-10 producing Th subsets in a time course study of collagen induced arthritis (CIA) animal models. We found that joint inflammation in CIA mouse peaked at 5 weeks after first immunization with CII, which was significantly subdued in mice pre-treated by repeated oral administration of CII. Orally tolerized mice also showed increase in their serum level of IgG1, while the level of IgG2a was decreased. T-cell proliferation upon CII stimulation was also suppressed in lymph nodes of mice given oral administration of CII compared to non-tolerized controls. When cultured in vitro in the presence of CII, T-cells isolated from orally tolerized mice presented higher proportion of $CD4^+IL-10^+$ subsets compared to non-tolerized controls. Interestingly, such increase in IL-10 producing cells were obvious first in Peyer's patch, then by 5 weeks after immunization, in mesenteric lymph node and spleen instead. This result indicates that a particular subset of T-cells with immune suppressive functions might have migrated from the original contact site with CII to inflamed joints via peripheral blood after 5 weeks post immunization.

• Korean Journal of Veterinary Research
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• v.54 no.2
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• pp.75-79
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• 2014

Bordetella (B.) bronchiseptica is a causative agent of swine atrophic rhinitis that promotes colonization of the mucous membrane of the swine nasal cavity by Pasteurella (P.) multocida. Mixed infection with B. bronchiseptica and P. multocida leads to growth inhibition of pigs, resulting in significant economic loss. There are many commercial vaccines for atrophic rhinitis, including B. bronchiseptica as a killed vaccine antigen (Ag). However, the immunogenicity of killed B. bronchiseptica Ag has not yet been elucidated; therefore, this study was conducted to investigate the immunogenicity of killed B. bronchiseptica Ag and the type of immune response it induces. In vitro assays using mouse spleen cells and flow cytometry revealed that B. bronchiseptica Ag induced high proliferation capability of lymphocytes, especially B lymphocytes, and the proliferating cells showed a significant response to interleukin (IL)-2. B. bronchiseptica Ag also enhanced the production of IL-12, a representative cytokine for cell-mediated immunity. In vivo experiments using mice showed that the injection of B. bronchiseptica Ag markedly induced Ag-specific antibody. Taken together, these results indicate that B. bronchiseptica Ag has high immunogenicity by itself.

• Safety and Health at Work
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• v.13 no.2
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• pp.248-254
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• 2022

Background: Occupational hazards in crop farms vary diversely based on different field operations as soil management, harvesting processes, pesticide, or fertilizer application. We aimed at evaluating the immunological status of crop farmers, as limited systematic investigations on immune alteration involved with crop farming have been reported yet. Methods: Immunological parameters including plasma immunoglobulin level, major peripheral immune cells distribution, and level of cytokine production from activated T cell were conducted. Nineteen grape orchard, 48 onion open-field, and 21 rose greenhouse farmers were participated. Results: Significantly low proportion of natural killer (NK) cell, a core cell for innate immunity, was revealed in the grape farmers (19.8±3.3%) in comparison to the onion farmers (26.4±3.1%) and the rose farmers (26.9±2.5%), whereas cytotoxic T lymphocyte proportion was lower in the grape and the onion farmers than the rose farmers. The proportion of NKT cell, an immune cell implicated with allergic response, was significantly higher in the grape (2.3±0.3%) and the onion (1.6±0.8%) farmers compared with the rose farmers (1.0±0.4%). A significantly decreased interferon-gamma:interleukin-13 ratio was observed from ex vivo stimulated peripheral blood mononuclear cells of grape farmers compared with the other two groups. The grape farmers revealed the lowest levels of plasma IgG1 and IgG4, and their plasma IgE level was not significantly different from that of the onion or the rose farmers. Conclusion: Our finding suggests the high vulnerability of workplace-mediated allergic immunity in grape orchard farmers followed by open-field onion farmers and then the rose greenhouse farmers.

• Journal of Life Science
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• v.23 no.3
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• pp.448-461
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• 2013

Inflammatory bowel disease, known as Crohn's disease and ulcerative colitis, is an unexplained disease characterized by chronic inflammation that repeats a cycle of relapse, improvement, and complications. The cause of inflammatory bowel disease is not clearly known, but it is predicted that a complex of various factors precipitate its occurrence. In particular, inflammatory mediators, such as cytokine, induce an increase in cell-mediated inflammatory responses. Focal tissue damage then occurs in the intestinal mucosa because of the weakening of the immune-modulating functions of cotton. Immune and inflammatory responses do not decrease appropriately but continue until they lead to chronic inflammation. Current research has focused on the cytokine genes, which have important roles in these inflammatory responses. Cytokine is a glycoprotein that is produced mostly in activated immune cells. It connects the activation, multiplication, and differentiation between immune cells, which causes focal tissue damage and inflammatory response. Moreover, butyrate, which originates in dietary fiber and plays an important role in the structure and function of the intestinal area, shows control functions in the intestinal immune system by decreasing the proinflammatory cytokine and increasing the anti-inflammatory cytokine. Therefore, this research investigated the molecular mechanism of the anti-inflammatory effects of butyrate to comprehend the cytokine controlling abilities of butyrate in the immune cells. Butyrate is expected to have potential in new treatment strategies for inflammatory bowel disease.