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Effects of Physical Training on Defence Mechanism of Aging and Memory Impairment of Senescence-accelerated SAMP8.

Woo Young KU ; Yi Sub KWAK ; Jong Soo LEE

Immune Network.2005;5(4):252-257. doi:10.4110/in.2005.5.4.252

BACKGROUND: This study was designed to investigate the effect of exercise training on defense mechanism of chronic degenerative disease, aging, and memory impairments of senescence-accelerated mouse (SAM)P8 under the hypothesis that "Senile dementia may be prevented by regular exercises". METHODS: To evaluate the effects of exercise training on the defense mechanism of aging and memory impairment, SAMP8 were divided into two groups, the control group and exercise training groups. the exercise training group were performed with low (O2max 25~33%), middle (O2max 50%) and high (O2max 66~75%) intensity exercise. All SAMP8 mice were fed experimental diet ad libitum until 4, 8 months, and dead period. RESULTS: Median lifespan in middle exercise group resulted in a significantly increased (23.5% and 18.7%, respectively), whereas these lifespan in high exercise group resulted in an unexpectedly decreased (13.5% and 12.1%, respectively) compared with control group. Body fat levels in 4 and 8 months of age were significantly decreased 43% to 51% in middle exercise group, whereas were remarkably deceased to 57% in high exercise group compared with control group. It is believed that extended median and maximum lifespan may be effected by calory restriction through the exercise training. Acetylcholine (ACh) levels were significantly increased 6.7% and 8.5% in middle and high exercise groups, and also choline acetyltransferase (ChAT) activities were significantly increased 10.3% and 11.9% in middle and high exercise groups. CONCLUSION: These results suggest that proper and regular exercises such as middle group (O2max 50%) may play an effective role in attenuating an oxygen radicals and may play an important role in improving a learning and memory impairments of senile dementia.
Acetylcholine ; Adipose Tissue ; Aging* ; Alzheimer Disease ; Animals ; Choline O-Acetyltransferase ; Dementia ; Diet ; Exercise ; Learning ; Memory* ; Mice ; Reactive Oxygen Species

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Inhibition of Cell Migration by Corticotropin-Releasing Hormone (CRH) in Human Natural Killer Cell Line, NK-92MI.

Soyoung CHEON ; Saik BANG ; Daeho CHO

Immune Network.2005;5(4):247-251. doi:10.4110/in.2005.5.4.247

BACKGROUND: Natural killer (NK) cells are CD3 (-) CD14 (-) CD56 (+) lymphocytes. They play an important role in the body's innate immune response. They can induce spontaneous killing of cancer cells or virus-infected cells via the Fas/Fas ligand or the granzyme/perforin systems. The corticotropin-releasing hormone (CRH) is an important regulator for the body's stress response. It promotes proliferation and migration of various cancer cells through the CRH type 1 receptor under stress, and also inhibits NK or T cell activity. However, the relationship of CRH and NK cell migration to the target has not been confirmed. Herein, we study the effect of CRH on NK cell migration. METHODS: We used the human NK cell line, NK-92MI, and tested the expression of CRH receptor type 1 on NK-92MI by RT-PCR. This was to examine the effect of CRH on tumor and NK cell migration, thus NK cells (NK-92MI) were incubated with or without CRH and then each CRH treated cell's migration ability compared to that of the CRH untreated group. RESULTS: We confirmed that CRH receptor type 1 is expressed in NK-92MI. CRH can decrease NK cell migration in a time-/dose-dependent manner. CONCLUSION: These data suggest CRH can inhibit NK cell migration to target cells.
Cell Movement* ; Corticotropin-Releasing Hormone* ; Homicide ; Humans* ; Immunity, Innate ; Killer Cells, Natural* ; Lymphocytes ; Receptors, Corticotropin-Releasing Hormone

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The Phospholipase-Protein Kinase C-MEK-ERK Pathway is Essential in Mycobacteria-induced CCL3 and CCL4 Expression in Human Monocytes.

Chul Su YANG ; Chang Hwa SONG ; Saet Byel JUNG ; Kil Soo LEE ; Su Young KIM ; Ji Sook LEE ; A Rum SHIN ; Jae Hee OH ; Yu Mi KWON ; Hwa Jung KIM ; Jeong Kyu PARK ; Tae Hyun PAIK ; Eun Kyeong JO

Immune Network.2005;5(4):237-246. doi:10.4110/in.2005.5.4.237

BACKGROUND: Little information is available on the identification and characterization of the upstream regulators of the signal transduction cascades for Mycobacterium tuberculosis (M. tbc)-induced ERK 1/2 activation and chemokine expression. We investigated the signaling mechanisms involved in expression of CCL3/MIP-1 and CCL4/MIP-1 in human primary monocytes infected with M. tbc. METHODS: MAP kinase phosphorylation was determined using western blot analysis with specific primary antibodies (ERK 1/2, and phospho-ERK1/2), and the upstream signaling pathways were further investigated using specific inhibitors. RESULTS: An avirulent strain, M. tbc H37Ra, induced greater and more sustained ERK 1/2 phosphorylation, and higher CCL3 and CCL4 production, than did M. tbc H37Rv. Specific inhibitors for mitogen-activated protein kinase (MAPK) kinase (MEK; U0126 and PD98059) significantly inhibited the expression of CCL3 and CCL4 in human monocytes. Mycobacteria-mediated expression of CCL3 and CCL4 was not inhibited by the Ras inhibitor manumycin A or the Raf-1 inhibitor GW 5074. On the other hand, phospholipase C (PLC) inhibitor (U73122) and protein kinase C (PKC)- specific inhibitors (GO6976 and Ro31-8220) significantly reduced M. tbc-induced activation of ERK 1/2 and chemokine synthesis. CONCLUSION: These results are the first to demonstrate that the PLC-PKC-MEK-ERK, not the Ras-Raf-MEK-ERK, pathway is the major signaling pathway inducing M. tbc-mediated CCL3 and CCL4 expression in human primary monocytes.
Antibodies ; Blotting, Western ; Hand ; Humans* ; Monocytes* ; Mycobacterium tuberculosis ; Phosphorylation ; Phosphotransferases* ; Protein Kinase C ; Protein Kinases ; Signal Transduction ; Type C Phospholipases

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The Effect of Different Type of Exercise on SOD, Neutrophils and T Lymphocytes.

Yi Sub KWAK ; Sang Yong UM ; Dong Eun KIM ; Hye Jin HWANG

Immune Network.2005;5(4):232-236. doi:10.4110/in.2005.5.4.232

BACKGROUND: A physically active lifestyle and regular exercise training incurs many health benefits. One recently recognized benefit of regular moderate exercise is stress reduction and immune enhancement. Thus, a physical stress such as exercise may act at any number of points in the complex sequence of events collectively termed the immune response. Although exercise causes many propound changes in parameters of immune function, the nature and magnitude of such changes rely on several factors including the immune parameters of interest; type, intensity, and duration of exercise; fitness level or exercise history of the subject; environmental factors such as ambient temperature and humidity. METHODS: This study was undertaken to investigate the effect of different type of exercise on superoxide dismutase (SOD), neutrophils, and T lymphocytes of Sprague-Dawley rats. Sprague-Dawley rats were randomly divided into three groups; a non-Trained group (NTG, n=6), a swim-Trained group (STG), and a treadmill-Trained group (TTG). The exercise regimen was designed in a treadmill (5 times/5 days/week) during 8-weeks for TTG, and swim training (5 times/5 days/week) during 8-weeks for STG, and the volume of exercise training was the same in both groups. RESULTS: 8 weeks of regular swim and treadmill training significantly increased liver SOD concentration however, muscle SOD concentration was not statistically significant. In the level of neutrophils, TTG and STG showed significant difference, compared to NTG. TTG was the highest level of neutrophils. In the level of immune cell counts, there was significant difference among TTG, STG, and NTG both in the spleen and thymus. Conculsion: In conclusion, it can be stated that eight weeks swim and treadmill exercise training has beneficial effect in improving immune response and antioxidant defence capacity by augmenting immune cells and SOD activities of SD rats.
Animals ; Cell Count ; Humidity ; Insurance Benefits ; Life Style ; Liver ; Neutrophils* ; Rats ; Rats, Sprague-Dawley ; Spleen ; Superoxide Dismutase ; T-Lymphocytes* ; Thymus Gland

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Exacerbation of Japanese Encephalitis by CD11c(hi) Dendritic Cell Ablation Is Associated with an Imbalance in Regulatory Foxp3⁺ and IL-17⁺CD4⁺ Th17 Cells and in Ly-6C(hi) and Ly-6C(lo) Monocytes.

Jin Young CHOI ; Jin Hyoung KIM ; Ajit Mahadev PATIL ; Seong Bum KIM ; Erdenebelig UYANGAA ; Ferdaus Mohd Altaf HOSSAIN ; Seong Kug EO

Immune Network.2017;17(3):192-200. doi:10.4110/in.2017.17.3.192

Japanese encephalitis (JE) is neuroinflammation characterized by uncontrolled infiltration of peripheral leukocytes into the central nervous system (CNS). We previously demonstrated exacerbation of JE following CD11c(hi) dendritic cell (DC) ablation in CD11c-DTR transgenic mice. Moreover, CD11c(hi) DC ablation led to abnormal differentiation of CD11b⁺Ly-6C(hi) monocytes and enhanced permeability of the blood-brain barrier (BBB), resulting in promoting the progression of JE. Here, we examined changes in lymphoid and myeloid-derived leukocyte subpopulations associated with pro- and anti-inflammation during JE progression. The analyses of this study focused on regulatory CD4⁺Foxp3⁺ regulatory T cells (Tregs), IL-17⁺CD4⁺ Th17 cells, and CD11b⁺Ly-6C(hi) and Ly-6C(lo) monocytes. CD11c(hi) DC ablation resulted in the accumulation of IL-17⁺CD4⁺ Th17 cells in the CNS, thereby leading to lower ratio of Tregs to Th17 cells. This result was corroborated by the higher expression levels of IL-17 and RORγT in CD4⁺ T cells from the brains of CD11c(hi) DC-ablated mice. In addition, CD11c(hi) DC-ablated mice showed higher frequency and total number of inflammatory CD11b⁺Ly-6C(hi) monocytes, whereas CD11b⁺Ly-6C(lo) monocytes were detected with lower frequency and total number in CD11c(hi) DC-ablated mice. Furthermore, CD11c(hi) DC ablation altered the phenotype and function of CD11b⁺Ly-6C(lo) monocytes, resulting in lower levels of activation marker and anti-inflammatory cytokine (IL-10 and TGF-β) expression. Collectively, these results indicate that CD11c(hi) DC ablation caused an imbalance in CD4⁺ Th17/Treg cells and CD11b⁺Ly-6C(hi)/Ly-6C(lo) monocytes in the lymphoid tissue and CNS during JE progression. This imbalanced orchestration of pro- and anti-inflammatory leukocytes following CD11c(hi) DC ablation may contribute to the exacerbation of JE.
Animals ; Asian Continental Ancestry Group* ; Blood-Brain Barrier ; Brain ; Central Nervous System ; Dendritic Cells* ; Encephalitis, Japanese* ; Humans ; Interleukin-17 ; Leukocytes ; Lymphoid Tissue ; Mice ; Mice, Transgenic ; Monocytes* ; Permeability ; Phenotype ; T-Lymphocytes ; T-Lymphocytes, Regulatory ; Th17 Cells*

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Moderate Exercise Enhances the Production of Interferon-γ and Interleukin-12 in Peripheral Blood Mononuclear Cells.

Alireza ZAMANI ; Iraj SALEHI ; Mahdi ALAHGHOLI-HAJIBEHZAD

Immune Network.2017;17(3):186-191. doi:10.4110/in.2017.17.3.186

The purpose of this study was to explore the effect of two months moderate exercise on levels of IFN-γ, IL-12, IL-6 and IL-4 in serum and supernatants of in vitro mitogen-activated (PHA for 48 h) whole blood (WB) and peripheral blood mononuclear cells (PBMCs). Sixteen healthy males participated in running program (30 min/day, 5 days/week). Blood samples were collected in three stages; 24 h before to start exercise, 48 h and two months after the last session of the exercise. The samples were analyzed for the cytokines by ELISA. The levels of IFN-γ and IL-12 were increased significantly in activated PBMCs culture after exercise and were back to normal level after two months rest. A significant elevation of IFN-γ/IL-4 ratio was observed in activated PBMCs culture by acting possibly on IFN-γ. The results suggest that short moderate intensity exercise enhances Th1 immune inflammatory and anti-allergic conditions in response to mitogen.
Cytokines ; Enzyme-Linked Immunosorbent Assay ; Humans ; In Vitro Techniques ; Inflammation ; Interleukin-12* ; Interleukin-4 ; Interleukin-6 ; Male ; Running

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Diclofenac Inhibits 27-hydroxycholesterol-induced Differentiation of Monocytic Cells into Mature Dendritic Cells.

Yonghae SON ; Bo Young KIM ; Young Chul PARK ; Koanhoi KIM

Immune Network.2017;17(3):179-185. doi:10.4110/in.2017.17.3.179

We investigated whether diclofenac could influence the development of antigen-presenting cells in an oxygenated cholesterol-rich environment by determining its effects on the 27-hydroxycholesterol (27OHChol)-induced differentiation of monocytic cells into mature dendritic cells (mDCs). Treatment of human THP-1 monocytic cells with diclofenac antagonized the effects of 27OHChol by attenuating dendrite formation and cell attachment and promoting endocytic function. Diclofenac inhibited the transcription and surface expression of the mDC markers of CD80, CD83, and CD88, and reduced the 27OHChol-induced elevation of surface levels of MHC class I and II molecules to the basal levels in a dose-dependent manner. It also reduced the expression of CD197, a molecule involved in DC homing and migration. These results indicate that diclofenac inhibits the differentiation of monocytic cells into mDCs, thereby potentially modulating adaptive immune responses in a milieu rich in cholesterol oxidation products.
Antigen-Presenting Cells ; Cholesterol ; Dendrites ; Dendritic Cells* ; Diclofenac* ; Humans ; Oxygen

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Effects of Cellular 11β-hydroxysteroid Dehydrogenase 1 on LPS-induced Inflammatory Responses in Synovial Cell Line, SW982.

Young Sik CHO ; Ki Nam KIM ; Jung Hyun SHIM

Immune Network.2017;17(3):171-178. doi:10.4110/in.2017.17.3.171

11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) catalyzes the conversion of inactive cortisone into active cortisol, which has pleiotropic roles in various biological conditions, such as immunological and metabolic homeostasis. Cortisol is mainly produced in the adrenal gland, but can be locally regenerated in the liver, fat, and muscle. Its diverse actions are primarily mediated by binding to the glucocorticoid receptor. SW982, a human synovial cell line, expresses 11β-HSD type 1, but not type 2, that catalyzes the conversion of cortisone to cortisol. In this study, therefore, we investigated the control of lipopolysaccharide (LPS)-induced inflammatory responses by prereceptor regulation-mediated maintenance of cortisol levels. Preliminarily, cell seeding density and incubation period were optimized for analyzing the catalytic activity of SW982. Additionally, cellular 11β-HSD1 still remained active irrespective of monolayer or spheroid culture conditions. Inflammatory stimulants, such as interleukin (IL)-1β, tumor necrosis factor (TNF)α, and LPS, did not affect the catalytic activity of 11β-HSD1, although a high dose of LPS significantly decreased its activity. Additionally, autocrine effects of cortisol on inflammatory responses were investigated in LPS-stimulated SW982 cells. LPS upregulated pro-inflammatory cytokines, including IL-6 and IL-1β, in SW982 cells, while cortisol production, catalyzed by cellular 11β-HSD1, downregulated LPS-stimulated cytokines. Furthermore, suppression of NFκB activation-mediated pro-inflammatory responses by cortisol was revealed. In conclusion, the activity of cellular 11β-HSD1 was closely correlated with suppression of LPS-induced inflammation. Therefore, these results partly support the notion that prereceptor regulation of locally regenerated cortisol could be taken into consideration for treatment of inflammation-associated diseases, including arthritis.
Adrenal Glands ; Arthritis ; Cell Line* ; Cortisone ; Cytokines ; Homeostasis ; Humans ; Hydrocortisone ; Inflammation ; Interleukin-6 ; Interleukins ; Liver ; Oxidoreductases* ; Receptors, Glucocorticoid ; Tumor Necrosis Factor-alpha

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Clonal Expansion of Allergen-specific CD4⁺ T Cell in the Lung in the Absence of Lymph Nodes.

Garam CHOI ; Byung Seok KIM ; Young Jun PARK ; Inbo SHIM ; Yeonseok CHUNG

Immune Network.2017;17(3):163-170. doi:10.4110/in.2017.17.3.163

The expansion of allergen-specific CD4⁺ T cells is a critical step in inducing airway inflammation during allergic asthma. Such clonal expansion of T cells is initiated through the interaction between allergen-bearing dendritic cells and allergen-specific naïve T cells in the draining lymph nodes. Whether such T cell clonal expansion also occurs in the lung, the primary organ encountering inhaled allergens, remains unclear. Compared with wild-type mice, we found similar frequencies of CD4⁺ T cells in the lung of lymph node-deficient Rorgt(gfp/gfp) mice after repeated exposure to inhaled allergens. In addition, we observed an evident population of CD4⁺ T cells that underwent clonal expansion in the lung of allergen-challenged mice treated with an S1P antagonist FTY720 in an in vivo proliferation study with CFSE-labeled OT-II T cells. Moreover, the expansion of allergen-specific CD4⁺ T cells was significantly enhanced in the lungs of Rorgt(gfp/gfp) mice in comparison to that of wild-type mice. These results together demonstrate that the clonal expansion of allergen-specific CD4⁺ T cells occurs in the absence of the lymph nodes, indicating that the lung can act as a primary site of the clonal expansion of CD4⁺ T cells in response to inhaled allergens.
Allergens ; Animals ; Asthma ; Dendritic Cells ; Fingolimod Hydrochloride ; Inflammation ; Lung* ; Lymph Nodes* ; Mice ; T-Lymphocytes

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Dendritic Cell Dysfunction in Patients with End-stage Renal Disease.

Ji Ung KIM ; Miyeon KIM ; Sinae KIM ; Tam Thanh NGUYEN ; Eunhye KIM ; Siyoung LEE ; Soohyun KIM ; Hyunwoo KIM

Immune Network.2017;17(3):152-162. doi:10.4110/in.2017.17.3.152

End-stage renal disease (ESRD) with immune disorder involves complex interactions between the innate and adaptive immune responses. ESRD is associated with various alterations in immune function such as a reduction in polymorphonuclear leukocyte bactericidal activity, a suppression of lymphocyte proliferative response to stimuli, and a malfunction of cell-mediated immunity at the molecular level. ESRD also increases patients' propensity for infections and malignancies as well as causing a diminished response to vaccination. Several factors influence the immunodeficiency in patients with ESRD, including uremic toxins, malnutrition, chronic inflammation, and the therapeutic dialysis modality. The alteration of T-cell function in ESRD has been considered to be a major factor underlying the impaired adaptive cellular immunity in these patients. However, cumulative evidence has suggested that the immune defect in ESRD can be caused by an Ag-presenting dendritic cell (DC) dysfunction in addition to a T-cell defect. It has been reported that ESRD has a deleterious effect on DCs both in terms of their number and function, although the precise mechanism by which DC function becomes altered in these patients is unclear. In this review, we discuss the effects of ESRD on the number and function of DCs and propose a possible molecular mechanism for DC dysfunction. We also address therapeutic approaches to improve immune function by optimally activating DCs in patients with ESRD.
Antigen-Presenting Cells ; Dendritic Cells* ; Dialysis ; Humans ; Immune System Diseases ; Immunity, Cellular ; Inflammation ; Kidney Failure, Chronic* ; Lymphocytes ; Malnutrition ; Neutrophils ; T-Lymphocytes ; Vaccination

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