• The Journal of the Korean dental association
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• v.18 no.1 s.130
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• pp.55-58
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• 1980

치주질환 발생시의 대식세포의 형태적 변화 및 기능적인 상관관계를 연구하고저 성견 5마리를 사용 실험하였다. 실험동물을 전신마취한 후 상하악 우측 제 1 및 제 2 소구치의 치경부에 1.3mm굵기의 wire를 4주간 결찰하여 인위적으로 치주염을 유발시켜 실험적으로 하였고, 동일동물의 좌측 제 1 및 제 2 소구치를 대조군으로 하였다. 실험군 및 대조군의 치아협측치은을 0.5 0.5 1mm의 형태로 절제하여 전자현미경적 관찰을 위한 통법의 조직처리를 한 다음 관찰하였다. 그 관찰 결과를 보면 다음과 같았다. 1. 실첨군의 치은의 고유층에 탐식성 돌기를 가진 많은 대식세포들이 출현하였다. 2. 변성된 교원 섬유군 인접부위에 phagocytic vesicle을 가진 대식세포들의 세포질내에 지방과립 및 잔존물을 볼 수 있었다. 한편 RER 및 Golgi complex는 매우 적었다. 3. 세포막은 그 기능상으로 많은 ruffles or folds를 나타냈으며 이 물질을 포식하는 양식을 뛰기도 하였다. pinocytotic activity를 띄는 대식세포들도 보였다. 4. 신생섬유아세포 주위에 밀접한 관계를 띄고 대식세포가 나타났으며 상호 유사하다. 대식세포에는 많은 residual body가 나타났고 RER은 매우 적었다.

• Parasites, Hosts and Diseases
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• v.28 no.2
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• pp.85-90
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• 1990

This study was aimed to observe the direct and Iymphokine-activated cell mediated cytotoxic effects against Trichomenas waginalis by mouse peritoneal macrophages. Cytotoxicity was measured as release of 3H-thymidine from prelabeled protozoa, and tested in U-bottom microtiter plates. A 0.1 ml suspension of labeled protozoa (2{\times}10^5/ml$) was placed in each well, followed by 0.1 ml of a suspension containing increasing numbers of peritoneal cells. After a 24 hr incubation at $37^{\circ}C$, 0.1ml of the supernatant was collected and counted in liquid scintillation counter. Mouse peritoneal macrophages had appreciable level of spontaneous cytotoxicity against T. maginalis at the effector to target cell ratios from 5 : 1 to 50 : 1, Treatment of macrophages with Iymphokine, produced by PHA-stimulated spleen cells, increased the cytotoxicity in comparison with resident macrophages against T. vaginalis. The degree of macrophage activation for the killing was not dependent upon the Iymphokine concentration. Peritoneal cells adherent to plastic displayed significant levels of cytotoxicity against T. vaginalis. This study indicates that mouse peritoneal macrophages are spontaneously cytotoxic for T. waginalis and Iymphokine increases the cytotoxicity by activating macrophages to kill T. vaginalis.

• Korean Journal of Acupuncture
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• v.26 no.3
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• pp.69-76
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• 2009

Objectives : 본 연구의 목적은 제습, 해독, 통리관절등의 효능이 있는 토복령이 RAW264.7 대식세포주에서 lipopolysaccharide(LPS)로 처치하여 생성되는 nitric oxide(NO)와 prostaglandin $E_2$($PGE_2$)에 억제작용이 있는지 관찰하고자 하는 것이다. Methods : 토복령이 RAW264.7 대식세포주에 세포독성이 유무를 관찰하기 위하여 농도별 MTT assay를 수행하여 세포생존율을 측정하였다. 또한 LPS로 염증유발된 RAW264.7 대식세포주에서 토복령의 농도별 처치가 NO 및 $PGE_2$ 생성억제에 미치는 영향을 관찰하고자 NO 및 $PGE_2$ assay를 수행하였다. Results : 토복령의 농도별 처치가 RAW264.7 대식세포주에서 세포독성을 유발하는지 MTT assay로 측정한 결과 세포독성은 관찰되지 않았으며, 토복령은 LPS처치로 인하여 증가된 NO 및 $PGE_2$ 생성을 통계학적으로 유의하게 감소시킴을 관찰하였다. Conclusions : 본 연구를 통하여 토복령은 RAW264.7 대식세포주에서 LPS로 유도된NO 및 $PGE_2$ 생성을 효과적으로 억제시킴으로써 추후 염증질환의 치료제로서 가능성을 확인하였다.

• Journal of Life Science
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• v.27 no.8
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• pp.873-878
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• 2017

We previously reported that NAD(P)H:quinone oxidoreductase 1 (NQO1)-knockout (KO) mice exhibited spontaneous inflammation in the gut. We also found that NQO1-KO mice showed highly increased inflammatory responses compared with NQO1-WT control mice when subjected to DSS-induced experimental colitis. In a Clostridium difficile toxin-induced mouse enteritis model, NQO1-KO mice were also sensitive compared with NQO1-WT mice. Moreover, numerous studies have shown that NQO1 is functionally associated with immune regulation. Here, we assessed whether NQO1 defects can alter macrophage activation. We found that peritoneal macrophages isolated from NQO1-KO mice produced more IL-6 and $TNF-{\alpha}$ than those isolated from NQO1-WT mice. Moreover, the dicumarol-induced inhibition of NQO1 significantly increased IL-6 and $TNF-{\alpha}$ production in peritoneal macrophages isolated from NQO1-WT mice, as well as in the cultured mouse macrophage cell line, RAW264.7. These results indicate that NQO1 may negatively regulate the activation of macrophages. Knockout or chemical inhibition of NQO1 markedly reduced the expression of $I{\kappa}B$ (inhibitor of $NF{\kappa}B$) in both mouse peritoneal macrophages and RAW264.7 cells. Finally, RAW264.7 cells treated with dicumarol exhibited morphological changes reflecting macrophage activation. Our results suggest that NQO1 may suppress the $NF{\kappa}B$ pathways in macrophages, thereby suppressing the activation of these cells. Thus, immunosuppressive activity may be among the many possible functions of NQO1.

• Parasites, Hosts and Diseases
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• v.35 no.3
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• pp.189-196
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• 1997

The purpose of this study is to determine whether nitric oxide is involved in the extracellular killing of Trichomoncs uasinalis by mouse (BALB/c) peritoneal macrophages and RAW264.7 cells activated with LPS or rIFN-γ and also to observe the effects of various chemicals which affect the production of reactive nitrogen intermediates (RNl) in the cytotoxicity against T. vnginnlis. The cytotoxicity was measured by counting the release of (3H)-thymidine from labelled protozoa and NOa was assayed by Griess reaction. Nemonomethyl-L-arginine (L-NMHA), Nenitro-L-arginine methyl ester (NAME) and arginase inhibited cytotoxicity to T. vaginnlis and nitrite production by activated mouse perioneal macrophagrs and RAW 264.7 cells. The addition of excess L-arginine competitively restored trichomonacidal activity of macrophages. Exogenous addition of FeSO4 inhibited cytotoxicity to T. vaginaLis and nitric products of macrophages. From above results, it is assumed that nitric oxide plays an important role in the host defense mechanism of macrophages against T ucfinalis.

• Journal of Korean society of Dental Hygiene
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• v.13 no.1
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• pp.174-180
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• 2013

연구목적 : 자극성 섬유종은 만성자극에 의해 발생하는 구강내 증식성 병변이다. 상처치유의 초기 과정에서는 비만 세포와 대식 세포가 섬유모세포의 이주, 증식, 아교질합성 등에 연관되어 있는 성장인자와 사이토카인을 분비하여 상처 치유에 중요한 역할을 한다. 저자들은 자극성 섬유종을 조직학적 특성에 따라 세분하고, 각각의 조직학적 아형에서 비만 세포와 대식 세포의 발현을 조사하여 자극성 섬유종의 발생 기전을 이해하고자 하였다. 연구방법 : 본 연구에서는 82예의 자극성 섬유종을 조직 소견에 따라 4가지 유형으로 분류하였으며, 자극성 섬유종과 10예의 정상 구강점막에 톨루이딘 블루 염색과 CD 68 면역조직화학염색을 시행하였다. 이를 통계화하여 자극성 섬유종의 조직학적 아형에 따른 비만 세포와 대식 세포의 분포 정도를 관찰하였다. 연구결과 : 통계 결과 비만 세포와 대식 세포의 분포는 자극성 섬유종에서 현저히 증가하였으며, Spearman 상관계수는 0.693이었다. 결론 : 조직의 섬유화에 관여하는 비만 세포는 자극성 섬유종의 cellular type에서 유의하게 증가하였으며, 대식 세포도 자극성 섬유종의 모든 아형에서 유의하게 증가하였다. 따라서 자극성 섬유종의 형성 과정에는 비만 세포와 대식 세포의 증가가 중요한 역할을 하는 것으로 생각되었다.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.513-520
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• 1994

Background: The pathogenesis of silicosis has been focused on the interaction between alveolar macrophages and silica particle. Although fibrosis in silicosis has been studied extensively, the mechanism is still not fully understood. There is increasing evidence that monokines and arachidonic acid metabolites macrophage are involved in pathogenesis of silicosis. Recently, it was reported that prostaglandin E2 produced from macrophage counteracts the stimulatory effects of other monokines on fibroblast proliferation or collagen production. Until now, it was remained uncertain by which mechanism silica particle may activate alveolar macrophage to an enhanced release of prostaglandin E2. Methods: In order to investigate the relationship between the activity of alveolar macrophage and the production of $PGE_2$ from activated alveolar macrophage, the authors measured hydrogen peroxide and $PGE_2$ from alveolar macrophages activated by silica in vitro and from alveolar macrophages in the silicotic nodules from rat. Experimental silicosis was induced by intratracheal infusion of silica($SiO_2$) suspended in saline(50 mg/ml) in Sprague-Dawley rats. Results: produced by 1) The silicotic nodules with fibrosis were seen from the sections of rat lung at 60 days after intratracheal injection with 50 mg aqueous suspension of silica(Fig. 1). 2) In vitro, silica caused the dose dependent increase of hydrogen peroxide(p<0.05, Fig. 2A) and $PGE_2$(p>0.05, Fig. 2B) release from alveolar macrophages. Alveolar macrophages from rat with silicotic nodules released more hydrogen peroxide and $PGE_2$ than those of control group(p<0.05, Fig. 3). Conclusion: These results suggest that silica particle could activate macrophage directly and enhanced the release of $PGE_2$ and hydrogen peroxide from the alveolar macrophage.

• The Journal of Natural Sciences
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• v.8 no.2
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• pp.27-34
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• 1996

The phagocytosis and chemotaxis of murine macrophages after treated with saponin fractions are investigated. Phagocytic appearance against yeast was photographed by dying with Wright-Giemsa. Phagocytic activity of peritoneal macrophage was invreased in diol saponin treatment by 48% and was decreased in total saponin treatment by 35%. The ingestion of alveolar macrophage was increased by 50% maximally. Peritoneal chemotactic activity was shown in 17% increases and only diol saponin had effect in alveolar macrophage by 16%. According to SDS-PAGE method the contents of actin did not show any alterations.

• Tuberculosis and Respiratory Diseases
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• v.39 no.6
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• pp.526-535
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• 1992

Background: The oxygen radicals released by alveolar macrophages contribute to killing of microorganisms including M. tuberculosis. Macrophages are "primrd" for enhanced oxygen radical release by macrophage activator like IFN-$\gamma$ and LPS, which do not themselves cause release of oxygen radicals. Actural production of oxygen radicals is "triggered" by phagocytosis or by exposure to chemical stimuli like PMA or FMLP. There has been debates about the priming effect of alveolar macro phages because they are exposed to usual environmental particles unlike blood monocytes. Therefore we examined priming effect of IFN-$\gamma$ in human alveolar macrophages comparing with that in blood monocytes and rat alveolar macrophages. And we observed the alterations of superoxide production in both human and rat alveolar macrophages after exposure to M. tuberculosis H37Ra bacilli itself and its lysate. Methods: Bronchoalveolar lavage fluid was processed to isolate alveolar macrophages by adherence and the adherent cells were removed by cold shock method. After exposure to M. tuberculosis H37Ra strain, alveolar macrophages were incubated for 24 hours with IFN-$\gamma$. The amount of superoxide production stimulated with PMA was measured by ferricytochrome C reduction method. Results: 1) The priming effect in human alveolar macrophages was not observed even with high concentration of IFN-$\gamma$ while it was observed in blood monocytes and rat alveolar macrophages. 2) Both human and rat alveolar macrophages exposed to avirulent H37Ra strain showed triggering of superoxide release and similar results were shown with the exposure to H37Ra lysate. Conclusion: The priming effect in human alveolar macrophages is not observed because of its usual exposure to environmental particles and avirulent H37Ra strain does not inhibit the activation of alveolar macrophages.

• Parasites, Hosts and Diseases
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• v.29 no.2
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• pp.129-138
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• 1991

Tetrahymena pyriformis is a free-living ciliate protozoan in the freshwater system. Experiments were carried out to determine whether intraperitoneal administration of T. pyriformis (GL strain) to mice activates macrophages to be able to kill Toxoplasma gondii tachyzoites in vitro. Mice were also injected intraperitoneally with several synthetic activators; dimethyldioctadecylammonium bromide (DDA), dextran sulfate, complete Freund's adjutant (CFA) as well as Toxoplasma and Tetrehymena Iysates in order to activate mouse peritoneal macrophages. One week after the administration of activators, peritoneal cells were harvested and the adherent macrophages were challenged with Toxoplasma tachyzoites. Macrophage monolayers were then fixed with absolute methanol after washing, and stained with Giemsa solution. The percentage of the adherent cells infected and total number of organisms per 100 macrophages were calculated to make toxoplasma-cidal activity of macrophages according to the cultivation time. Peritoneal macrophages from mice administered with Tetrahymena exhibited significant protection against target parasites as compared with those treated with synthetic activators. Among non-biological synthetic activators, DDA was evaluated as an ellcellent activator.