• International Journal of Oral Biology
• /
• v.41 no.2
• /
• pp.83-88
• /
• 2016

Periodontitis is an inflammatory disease, which destroys the connective tissue and the alveolar bone. Recently, it has been suggested that the effect of natural substances could be induced into an anti-inflammatory environment. However, the effect of Safflower seed extract (SAF-M) associated with periodontitis has not been investigated yet. Therefore, the purpose of this study was to assess the anti-inflammatory effects of SAF-M. Cytotoxicity was assessed through MTS analysis using hGF and hPDL cells. Periodontitis was induced by injecting LPS into gingival tissue on the maxillary molars of rats ($45{\mu}g$ LPS/one time, 3 times a week for 3 weeks). SAF-M was administered daily at 30 mg/kg and 100 mg/kg. Alveolar bone resorption was evaluated through the micro-CT. hGF and hPDL cells showed differential cytotoxicity in response to SAF-M at 5 mg/ml and 1 mg/ml concentrations. Micro-CT showed reduction of the alveolar bone resorption in the SAF-M treatment group. These results suggested that SAF-M is a potential therapeutic agent for periodontitis.

• The Korean Journal of Cytopathology
• /
• v.17 no.1
• /
• pp.69-74
• /
• 2006

Alveolar soft part sarcoma (ASPS) is a rare soft tissue sarcoma, which occurs predominantly in adolescents and young adults. The cytological characteristics of this condition have been described only rarely in the literature. Here, we report a case of alveolar soft part sarcoma. A 28-year-old man presented with a mass in his right buttock, which had persisted for three years. The mass was subjected to a fine needle aspiration cytology (FNAC). The smears were cellular. The observed tumor cells were round or polygonal, and exhibited vesicular nuclei with prominent nucleoli and finely granular cytoplasm. Naked nuclei were frequently detected. Tumor cells were arranged singularly, but occasionally in a pseudoalveolar pattern.

• Journal of Periodontal and Implant Science
• /
• v.40 no.2
• /
• pp.61-68
• /
• 2010

Purpose: The present study was performed to clarify the relationship between periodontal disease severity and selected immunological parameters consisting of serum IgG titer against periodontopathogenic bacteria, the expression of the helper T-cell cytokine by gingival mononuclear cells, and patients' immunoreactivity to cross-reactive heat shock protein (HSP) epitope peptide from P. gingivalis HSP60. Methods: Twenty-five patients with moderate periodontitis had their gingival connective tissue harvested of gingival mononuclear cells during an open flap debridement procedure and peripheral blood was drawn by venipuncture to collect serum. The mean level of interproximal alveolar bone was calculated to be used as an index for periodontal disease severity for a given patient. Each of selected immunologic parameters was subject to statistical management to seek their correlations with the severity of periodontal disease. Results: A significant correlation could not be identified between serum IgG titers against specific bacteria (Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, Actinobacillus actinomycetemcomitans, and Streptococcus mutans) and the severity of periodontal disease. Expression of interleukin (IL)-10 by gingival mononuclear cells was statistically significant in the group of patients who had higher levels of alveolar bone height. However, a similar correlation could not be demonstrated in cases for IL-4 or interferon-$\gamma$. Patients' serum reactivity to cross-reactive epitope peptide showed a significant correlation with the amount of alveolar bone. Conclusions: It was concluded that expression of IL-10 by gingival mononuclear cells and patients' sero-reactivity to the cross-reactive HSP peptide of P. gingivalis HSP60 were significantly correlated with alveolar bone height.

• Toxicological Research
• /
• v.17 no.4
• /
• pp.255-265
• /
• 2001

Epidemiologic studies have demonstrated an association between short-term exposure to particulate air pollutants and increased mortality. However the biological mechanism underlying these associations have not been fully established and also the chemical and physical characteristics of the pollutant particles are not well understood. The metal constituents of air pollutant particles and their bioavailability are considered to Play an important role as possible mediators of Particle-induced airway injury and inflammation. Sprague-Dawley rat alveolar macrophage cells (NR8383) were exposed to airborne and acid-leached particulate matter (PM). Titanium oxide and nickel subsulfide were used as negative and positive controls. Particle-induced reactive oxygen species formation in cells was detected using the fluorescent probe 2',7'-dichlorofluorescin diacetate. Expression of TNF-$\alpha$ and IL-6 were measured by enzyme-linked immunosorbent assay, and PM-induced DNA double-strand breaks were determined with $\lambda$DNA/Hind III marker. Metals associated with air pollutant particles mediated intracellular oxidant production in alveolar macrophages, and the cytotoxicity and proinflammatory cytokine production induced by PM were associated with oxidative stress. The oxidants produced by air pollutant particles also are likely to induce DNA double-strand breaks. Our findings in alveolar macrophage cells exposed to PM and acid-leached PM support the hypothesis that metal components in urban air pollutants and their bioavailabilities might play an Important role in the induction of the adverse health effects.

• Korean Journal of Environmental Agriculture
• /
• v.28 no.3
• /
• pp.295-300
• /
• 2009

Formaldehyde (FA) is an important irritant compound in pesticide to induce asthma and allergy in respiratory system. Alveolar macrophage is also an pivotal cell in the immune response of respiratory system. However, the effect of FA in macrophage cell viability has not been elucidated. Thus, this study was conducted to investigate the effect of FA on apoptosis in Raw 264.7 cells, alveolar macrophage cell line. In this study, FA decreased cell viability of lung alveolar macrophage cells in a dose-dependent manner (>$100{\mu}M$). FA-induced decrease of cell viability was blocked by the treatment of antioxidants (vitamin C, NAC, and catalase). Indeed, FA induced lipid peroxide formation in Raw 264.7 cells. FA decreased Bcl-2 expression but increased Bax expression in lung alveloar macrophage cells. In addition, FA also increased the cleaved form of caspase-3. In conclusion, FA induced apoptosis via oxidative stress in cultured Raw 264.7 cells.

• Development and Reproduction
• /
• v.26 no.4
• /
• pp.155-163
• /
• 2022

Human pluripotent stem cells (hPSCs) can give rise to a vast array of differentiated derivatives, which have gained great attention in the field of in vitro toxicity evaluation. We have previously demonstrated that hPSC-derived alveolar epithelial cells (AECs) are phenotypically and functionally similar to primary AECs and could be more biologically relevant alternatives for assessing the potential toxic materials including in fine dust and cigarette smoking. Therefore, in this study, we employed hPSC-AECs to evaluate their responses to exposure of various concentrations of diesel particulate matter (dPM), cigarette smoke extract (CSE) and nicotine for 48 hrs in terms of cell death, inflammation, and oxidative stress. We found that all of these toxic materials significantly upregulated the transcription of pro-inflammatory cytokines such as IL-1α, IL-β, IL-6, and TNF-α. Furthermore, the exposure of dPM (100 ㎍/mL) strongly induced upregulation of genes related with cell death, inflammation, and oxidative stress compared with other concentrations of CSE and nicotine. These results suggest that hPSC-AECs could be a robust in vitro platform to evaluate pulmotoxicity of various air pollutants and harmful chemicals.

• The Korean Journal of Cytopathology
• /
• v.11 no.2
• /
• pp.115-119
• /
• 2000

Alveolar soft part sarcoma is a rare soft tissue tumor. Few cases on fine needle aspiration cytology have been reported in the literature. We experienced a case of recurrent alveolar soft part sarcoma of the right thigh diagnosed by fine needle aspiration cytology in a 47-year-old man. Cytologic findings showed single cells and clusters associated with thin wailed vasculature in a distinct pseudo-alveolar pattern. The tumor cells exhibited round or ovoid abundant granular cytoplasm and large pleomorphic nuclei with prominent central nucleoli.

• International Journal of Oral Biology
• /
• v.41 no.1
• /
• pp.33-38
• /
• 2016

One of functions of Galla Rhois (GR) is reportedly an anti-inflammatory effect on the several inflammatory diseases. However, an effect of GR related to periodontitis has not been investigated. In the present study, we examined the effect of the hexane extract of Galla Rhois (GR-H) on periodontitis. Cytotoxicity was assessed by MTS analysis using human gingival fibroblast (hGF) cells. Experimental periodontitis was induced by injecting E.coli LPS into the palatal gingiva maxillary molar thrice weekly for 3 weeks (LPS group). GR-H diluted in 1xPBS was orally administrated using a syringe at 30 mg/kg body weight and 100 mg/kg body weight once a day (GR-H group). GR-H effect on the alveolar bone loss (ABL) was digitized with a micro-CT. GR-H treatment at concentrations exceeding 0.5 mg/ml showed cytotoxic effect in hGF cells. The micro-CT among groups were presented for the different distances from cemento-enamel junction (CEJ) to alveolar bone crest (ABC). The results indicated an inhibitory effect on alveolar bone loss for orally administered GR-H in a model of LPS-induced periodontitis.

• Tuberculosis and Respiratory Diseases
• /
• v.42 no.4
• /
• pp.447-454
• /
• 1995

Cytokine release from alveolar macrophages and subsequent interaction of these cytokines with the bronchial epithelium can induce epithelial cells to release inflammatory mediators. Nitric oxide(NO), a highly reactive gas formed from arginine by nitric oxide synthase(NOS), is known to be involved in inflammation and edema formation, and the inducible form of NOS(iNOS) can be increased by cytokines. In this context, we hypothesized that lung epithelial cells could be stimulated by cytokines released by alveolar macrophages to express iNOS. To test this hypothesis, the murine lung epithelial cell line, LA-4, or the human lung epithelial cell line, A549, were stimulated with culture supernatant fluids from alveolar macrophages. NO production was assessed by evaluating the culture supernatant fluids for nitrite and nitrate, the stable end products of NO. Both murine and human cell culture supernatant fluids demonstrated an increase in nitrite and nitrate which were time- and dose-dependent and attenuated by $TNF{\alpha}$ and IL-$1{\beta}$ antibodies(p<0.05, all comparisons). Consistent with these observations, cytomix a combination of $TNF{\alpha}$, IL-$1{\beta}$, and $\gamma$-interferon, stimulated the lung epithelial cell lines as well as primary cultures of human bronchial epithelial cells to increase their NO production as evidenced by an increase in nitrite and nitrate in their culture supernatant fluids, an increase in the iNOS staining by immunocytochemistry, and an increase in iNOS mRNA by Northern blottin(p<0.05, all comparisons). The cytokine effects on iNOS were all attenuated by dexamethasone. To determine if these in vitro observations are reflected in vivo, exhaled NO was measured and found to be increased in asthmatics not receiving corticosteroids. These data demonstrate that alveolar macrophage derived cytokines increase iNOS expression in lung epithelial cells and that these in vitro observations are mirrored by increased exhaled NO levels in asthmatics. Increased NO in the lung may contribute to edema formation and airway narrowing.

• Tuberculosis and Respiratory Diseases
• /
• v.70 no.6
• /
• pp.462-473
• /
• 2011

Background: Smoking is a risk factor for idiopathic pulmonary fibrosis (IPF), but the mechanism of the association remains obscure. There is evidence demonstrating that plasminogen activator inhibitor-1 (PAI-1) is involved in the progression of pulmonary fibrosis. This study was to determine whether the administration of small interfering RNA (siRNA) targeting PAI-1 or PAI-1 inhibitor to the cigarette smoking extract (CSE)-exposed rat alveolar type II epithelial cells (ATII cells) limits the epithelial-mesenchymal transition (EMT). Methods: ATII cells were isolated from lung of SD-rat using percoll gradient method and cultured with 5% CSE. The EMT was determined from the ATII cells by measuring the real-time RT PCR and western blotting after the PAI-1 siRNA transfection to the cells and after administration of tiplaxtinin, an inhibitor of PAI-1. The effect of PAI-1 inhibitor was also evaluated in the bleomycin-induced rats. Results: PAI-1 was overexpressed in the smoking exposed ATII cells and was directly associated with EMT. The EMT from the ATII cells was suppressed by PAI-1 siRNA transfection or administration of tiplaxtinin. Signaling pathways for EMT by smoking extract were through the phosphorylation of SMAD2 and ERK1/2, and finally Snail expression. Tiplaxtinin also suppressed the pulmonary fibrosis and PAI-1 expression in the bleomycin-induced rats. Conclusion: Our data shows that CSE induces rat ATII cells to undergo EMT by PAI-1 via SMAD2-ERK1/2-Snail activation. This suppression of EMT by PAI-1 siRNA transfection or PAI-1 inhibitor in primary type II alveolar epithelial cells might be involved in the attenuation of bleomycin-induced pulmonary fibrosis in rats.