• Tuberculosis and Respiratory Diseases
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• v.47 no.2
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• pp.161-171
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• 1999

Background: Interleukin-12 (IL-12) can induce antitumor effects in vivo. This antitumor effect is associated with T cell infiltration but the effect of IL-12 on the steps of T cell migration into the tumor tissue has not been fully elucidated. This study focused on the effect of IL-12 on the tumor growth and the metastasis and on the expression of E-selectin, an adhesion molecule which is activated endothelial specific in its expression. In addition, we studied whether the expression of E-selectin is associated with the TNF-$\alpha$, a cytokine that its production is increased by IL-12 and has functions inducing a variety of adhesion molecules. Methods: Mice of C57BL/6 strain were injected with Lewis lung cancer cells followed by either IL-12, TNF-$\alpha$, or normal saline by intraperitoneal route. Twenty eight days after tumor cell inoculation, metastatic nodules of lung were enumerated and immunohistochemical staining of the subcutaneous tumors were performed with monoclonal antibodies to CD4, CD8, CD16, and E-selectin. In IL-12 treated mice, the subcutaneously implanted Lewis lung tumors were decreased in size and the metastases were also decreased in number compared to control mice. On tumor tissues, increased infiltration of CD4+, CD8+, and CD16+ cells were oberved in IL-12 treated mice compared to control mice. In control mice, E-selectin was absent on tumor vessels, but the expression of E-selectin was increased on tumor vessels of IL-12 treated mice. Administration of TNF-$\alpha$ increased not only the expression of E-selectin but also infiltrations of CD4+, CD8+, and CD16+ cells on tumor tissues. Conclusions: These results demonstrate that IL-12 inhibits tumor growth and metastases through infiltrations of inflammatory cells in mouse model of Lewis lung carcinoma and E-selectin may playa role in inflammatory cell recruitment on tumor tissue following IL-12 administration. Also, TNF-$\alpha$ may have a role as a mediator responsible for the IL-12 induced expression of E-selectin.

• Tuberculosis and Respiratory Diseases
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• v.50 no.6
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• pp.676-685
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• 2001

Background : Angiogenesis is an essential component of tumor growth and metastasis, and the vascular endothelial growth factor (VEGF) is one of the most important angiogenic factors. Several solid tumors produce substantial amounts of VEGF, which stimulates proliferation and the migration of endothelial cells, thereby inducing neovasculization by a paracrine mechanism. To evaluate the prognostic roles of angiogenesis and VEGF expression in patients with non-small cell lung cancer, the relationship between VEGF expression in tumor tissues, the clinicopathologic features and the overall survival rate were analysed. Methods : Sixty-nine resected primary non-small cell lung cancer specimens were evaluated. The paraffin-embedded tumor tissues were stained by anti-VEGF polyclonal antibodies using an immunohistochemical method to assess VEGF expression. Results : In Forty-one patients (59%), the VEGF antigen was expressed weakly in their tumor tissue, whereas in twenty-eight patients (41%) the VEGF antigen was expressed strongly. The median survival time of the weak VEGF expression group was 24 months, and that of the strong VEGF expression group was 19 months. The three year-survival rates were 35%, 33%, respectively. The survival difference between both groups was not statistically significant. Conclusion : Although results were not statistically significant, the strong expression group tended to poorer prognosis than the weak expression group.

• Journal of Life Science
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• v.30 no.10
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• pp.877-885
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• 2020

Lentinuls edodes has been used for traditional food and medicine around Asia, and a variety of biological effects have been reported. In this study, L. edodes water extract (LWE) was investigated for its anti-photodamage effect in HaCaT keratinocytes. To perform the necessary assays, L. edodes was extracted with distilled water for 8 hr at 40℃ in an extract tank. Anti-photodamage activity was assessed using a scratch wound healing assay, cell proliferation, and a reactive oxygen species (ROS) scavenging test and by measuring the mRNA and protein expression levels of matrix metalloproteinases (MMPs) and type I procollagen. MMPs and collagen expression are major markers of UV-induced photodamage in skin. Prior to photodamage analysis, the total polyphenol and β-glucan contents of the LWE were evaluated and found to be 4.64 mg GAE/g DW and 165.96 mg/g, respectively. Treatment with LWE induced cell migration and cell proliferation in UV-irradiated HaCaT cells, and LWE effectively scavenged the ROS induced by H₂O₂ and UVB irradiation in HaCaT cells. UVB irradiation induced ROS generation and led to increased production of MMP-1 and MMP-9 and to decreased collagen production in human keratinocytes. Treatment with LWE upregulated the expression levels of MMP-1, MMP-9, and type I procollagen in UVB-irradiated HaCaT cells. This study suggests that LWE could be used to develop cosmetic materials with anti-photodamage effects.

• Tuberculosis and Respiratory Diseases
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• v.43 no.4
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• pp.579-589
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• 1996

Background : Activation of neutrophil is critical for the clearance of microorganisms and toxic host mediators during sepsis. Unfortunately the activated neutrophil and its toxic byproducts can produce tissue injury and organ dysfunction. The leucocyte CD11/18 adhesion complex regulates neutrophil-endothelial cell adhesion, the first step in neutrophil migration to sites of injection and inflammation. To investigate the potential of neutrophil inhibition as a treatment strategy for sepsis, we evaluated the effects of monoclonal antibody against CD11b (MAb 1B6) in rats intrabronchial challenged with Escherichia coli. Methods : Animals were randomly assigned to receive monoclonal antibody against CD11b (1 mg/kg, sc) and bovine serum albumin(BSA, 1 mg/kg, sc) 6 hr before, at 0 and 6 hr after intrabronchial challenge of $20x10^9$ CFU/kg E. coli 0111. Animals were randomized to treat either 24, 60 or 90% oxygen after bacterial challenge and begining 4 hr after inoculation, all animals were received 100 mg/kg ceftriaxone qd for 3 days. Peripheral and alveolar neutrophil(by bronchoalveolar lavage) counts and lung injury parameters such as alveolar-arte rial $PO_2$ difference, wet to dry lung weight ratio and protein concentration of alveolar fluid were measured in survived rats at 12 hr and 96 hr. Results : Monoclonal antibody against CD11b decreased circulating and alveolar neutrophil especially more in 12 hr than in 96 hr The lung injury parameters of antibody-treated animals were not different from those of BSA-treated animals. but It was meaningless due to small number of survived animals. The early(6 hr) mortality rate was significantly increased in antibody-treated group(51%) compared to BSA-treated group(31%) (P=0.02) but late(from 12 hr to 72 hr) mortality rate was not different in antibody-treated group(44%) from BSA-treated group(36%) (P =0.089). Conclusion : Leucocyte CD11b/18 adhesion molecule is known to regulate neutrophil migration to the site of infection and inflammation. The monoclonal antibody against CD11b decreased alveolar neutrophil in rats with pulmonary sepsis and increased early mortality rate. Therefore, we can speculate that monoclonal antibody against CD11b blocks of alveolar recruitment of neutrophils, impairs host defense mechanism and increases early mortality rate of pulmonary sepsis in rat.

• Applied Microscopy
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• v.39 no.1
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• pp.27-40
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• 2009

Acute respiratory distress syndrome (ARDS), also known as an acute inflammatory lung disease is developed by various factors that is originated from the destruction of alveolar-capillary barrier, and neutrophils plays an important role in the destruction. The study intended to confirm, the anti-inflammatory effect of germanium, whether a lung injury has been mitigated with the reduction of injury in alveolar-capillary barrier resulting from inhibition of neutrophils migration in lung tissue. Test groups were divided in saline administered CON, 5 hours of endotoxin administered LPS and 5 hours of endotoxin administered Ge+LPS following 1 hours of pre-processed germanium. $100{\mu}g$ endotoxin was melted in 0.5 mL saline and sprayed into airway and 26 mg germanium per 100 g weight was administered into abdominal cavity. The endotoxin group which induced an acute lung injury with administered endotoxin showed dramatic increase of pulmonary edema (p<0.001), protein contents in bronchoalveolar lavage fluid, BALF (p<0.05) and neutrophils of infiltration in BALF (p<0.001) comparing with a control group, while a pre-treated germanium group showed significant decrease in all categories comparing to the endotoxin administerd group. In the result of a microscopic observation, the structure of alveolar-capillary barrier which is constructed with basal lamina, alveolar type I cells and endothelial cell were preserved of the pre-treated germanium group relatively well compare to the endotoxin administered group. And the construction of lamellar body, microvilli and basal lamina of alveolar type II cells were also preserved relatively well. Hence, germanium activates as an anti-Inflammatory mediator in other words, it interfered neutrophils migration into lung tissue, thereby reduced injury of alveolar-capillary barrier from toxic substances of activated neutrophils. Consequently, the study has determined that the acute lung injury induced by endotoxin has been decreased by the pre-treated germanium.

• Clinical and Experimental Pediatrics
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• v.51 no.8
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• pp.879-885
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• 2008

Purpose : The human lung fibroblast may act as an immunomodulatory cell by providing pro-inflammatory cytokines and chemokines, which are important in airway remodeling. Vascular endothelial growth factor (VEGF) induces mucosal edema and angiogenesis. Thymus and activation regulated chemokine (TARC) induces selective migration of T helper 2 cells. We investigated whether human lung fibroblasts produced VEGF and TARC, and the effects were augmented with the co-culture of fibroblasts and human bronchial smooth muscle cells (HBSMC), and whether dexamethasone can inhibit the proliferation and the release of VEGF in lung fibroblasts. Methods : Human lung fibroblasts were cultured with and without HBSMC, growth-arrested in serum-deprived medium, and pretreated with dexamethasone for 16 hours. After 24-hour stimulation with platelet derived growth factor-BB (PDGF-BB) and/or transforming growth factor-${\beta}$ (TGF-${\beta}$), culture supernatant was harvested for assays of VEGF and TARC. Cell proliferation was assayed using BrdU cell proliferation ELISA kit. Results : 1) The release of VEGF was significantly increased after stimulation with TGF-${\beta}$, and its release was augmented when co-stimulated with PDGF and TGF-${\beta}$. 2) VEGF release induced by PDGF or TGF-${\beta}$ was inhibited by dexamethasone. 3) There was no synergistic effect on the release of VEGF when human lung fibroblasts were co-cultured with HBSMC. 4) Dexamethasone did not suppress human lung fibroblasts proliferations. 5) Neither TGF-${\beta}$ nor PDGF induced TARC release from lung fibroblasts. Conclusion : Human lung fibroblasts may modulate airway remodeling by release of VEGF, but they have no synergistic effects when co-cultured with HBSMC. Dexamethasone suppresses VEGF release, not proliferation of lung fibroblast.

• Journal of Life Science
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• v.22 no.9
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• pp.1243-1253
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• 2012

The production and secretion of growth hormone (GH) in the anterior pituitary gland can be induced by several natural products to control cell proliferation, differentiation, and migration. To investigate whether Chungkookjang (CKJ) produced by the fermentation process affects GH-related metabolism, the secretion and the response of GH were observed in pituitary cells and GH target cells. Among six CKJs manufactured by different strains of glycine max, only three CKJs, including Daewon (DW), Daepung (DP), and Taegwang (TG), induced GH secretion from GH3 cells at 5.0 mg/ml concentration. There were no significant changes detected in the viability of any of the cells treated with these CKJs. In addition, the increase in GH secretion from the GH3 cells was dependent on the concentration of the three types of CKJs. The proliferation of cell lines, including MG63 and HepG2 cells, that originated from those derived from the GH target organs was significantly activated by treatment with the GH-containing conditional medium (GCM) harvested from the three CKJ-treated GH3 cells, although their induction rate was different from each other. In these cells, p-STAT5 was maximally translocated into the nucleus of MG63 cells 30 min after DW treatment, while it was translocated in HepG2 cells at 60 min. These results suggest that these three types of CKJ could enhance the secretion of GH, as well as the GCM-derived response, in the two target organs.

• Journal of Life Science
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• v.21 no.10
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• pp.1401-1406
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• 2011

Morphological changes in immune cells occur due to pathogen infection and natural circulation. T cells produce uropod, filopodia, lamellipodia, and microvilli for inflammation, immunosurvelliance, migration, and diapedesis. Short finger-like microvilli cover the surfaces of circulating mammalian immune cells. The surface features of monocytes and neutrophils are quite different, containing membrane ruffles as their predominant structure. In this study, we present the involvement of actin cytoskeleton regarding T lymphocyte microvilli. From analysis of scanning electron micrographs, Jurkat T lymphocyte microvilli was observed to rapidly disassemble when exposed to the actin-sequestering molecule, cytochalasin D. In contrast to cytochalasin D treatment, we found that median microvillar thickness was enlarged on Jurkat T lymphocytes treated with PMA via Lin-11, Isl-1, Mec-3 Kinase (LIMK) and cofilin signaling. In addition, actin cytoskeleton was involved in polarity formation in EL4 T lymphocytes. These results suggest that microvilli formation or polarity of T lymphocytes are involved in actin cytoskeleton dynamics.

• The korean journal of orthodontics
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• v.24 no.3 s.46
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• pp.673-693
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• 1994

Most adults, unlike growing children, have some periodontal problems which can influence the outcome of the orthodontic treatment. In cases where periodontal disease progression resulted in marked reduction of periodontium, orthodontic treatment could result in the worsening of the periodontal conditions, and therefore orthodontic treatment planning in such adult patients requires special considerations for the periodontal problems. This study investigates the effects of horizontal orthodontic tooth movement on the changes in the mesial, distal and furcation areas of the disease affected periodontium of adult dogs with advanced bone loss. Six adult dogs with healthy periodontium were selected, and mandibular 2nd premolars were extracted. In the mandibular 3rd premolars, angular bony defects in the mesial and distal sides, and horizontal bony defects in the furcation areas were created. Those that received the flap operation and plaque control were designated as the control, those that had horizontal tooth movement without plaque control after the flap operation as Experimental group I, those that had horizontal tooth movement under plaque control without the flap operation as Experimental group II, and those that had horizontal tooth movement under plaque control after the flap operation as Experimental group III. The control group was sacrificed 2 months postoperatively, and the experimental groups were sacrificed 5 months after the initiation of tooth movement. Specimens were histologically analyzed under light microscope. The results were as follows; 1. After the horizontal tooth movements, Experimental group I and II showed angular bony defects in the mesial sides of the roots and the distal side of the furcation areas, which correspond to the pressure sides. 2. After the horizontal tooth movements, Experimental group I and II showed decreased level of alveolar bone crest in the distal sides of the roots, which correspond to the tension sides. 3. Long junctional epithelium in the control group has not been replaced by periodontal connective tissue after the horizontal tooth movements. 4. Limited formation of new bone was observed in the angular bony defects in the mesial and distal aspects of the roots in the control group. 5. Inflammatory cell infiltration in the connective tissue was most severe in the Experimental group I, followed by Experimental group II, III, and the control group in that order. These results seem to indicate that plaque control was the most influencing factor in the alteration of the periodontal tissue after the horizontal tooth movements in the periodontal tissue with alveolar bone defects.

• The Journal of Korean Academy of Prosthodontics
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• v.54 no.3
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• pp.203-209
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• 2016

Purpose: Stimulating the proliferation and migration of periodontal ligament cells (PDLCs) has become the main goal of periodontal regeneration. To accomplish this goal, regeneration procedures have been developed, but results have not been predictable. Recently, tissue engineering using enamel matrix derivatives (EMDs) and growth factors has been applied to periodontal regeneration; however, the mechanism of EMDs is largely unknown. The aim of this study was to investigate the effects of EMDs on the proliferation and release of growth factors from PDLCs. Materials and methods: Human PDLCs were removed from individually extracted 3rd molars of healthy young adults, and cultured in the media containing EMDs (Emdogain, Biora, Malmo, Sweden) at concentration of 0, 12.5, 25, 50, 100, and $200{\mu}g/mL$ each. Cell proliferation and ALP (alkaline phosphatase) activity were measured. The evaluation of growth factors released by PDLCs was also performed by one-way analysis of variance (ANOVA) and Bonferroni's multiple comparison test. Results: Significantly increased proliferation and ALP activity were observed in PDLCs treated with over $25{\mu}g/mL$ and $50{\mu}g/mL$ EMDs, respectively. Additionally, treatment of PDLCs with $50{\mu}g/mL$ resulted in significantly increased release of vascular endothelial growth factor (VEGF) and transforming growth factor $(TGF)-{\beta}$ after 24 h and 48 h, respectively. Conclusion: EMDs enhance the proliferation and ALP activity of PDLCs, and promote the release of growth factors, including VEGF and $TGF-{\beta}$, from PDLCs. Therefore EMDs could be one of the effective methods for periodontal regeneration.