• 미생물학회지
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• 제32권4호
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• pp.280-284
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• 1994

공생 아메바에서 리소솜과 공생낭 간에 융합이 저해되는 이유로서는 먼저 이들 공생낭의 막에 어떤 특별한 인자가 존재하여 융합을 저해하거나 또는 융합 과정에 필수적인 어떤 요소가 이들 공생막에는 부족하여 융합이 일어나지 않는다고 유추해 볼 수 있다. 단일 클론 항체를 추적물질로 사용하여 이들 인자나 구성요소를 알아내는 과정에서, lipopolysaccharides가 공생 박테리아에 의하여 생산되어 공생낭의 막에 삽입된다는 것을 확인하였으며 이들이 공생막상에서도 세포질 방향으로 노출되어 있다는 것을 알아내었다. 따라서 이들 lipopolysaccharides가 리소솜과 공생낭간의 융합 저해에 간여하는 가를 알아보기 위하여 이들에 대한 단일 크론 항체를 공생 아메자의 세포질에 미세주사하여 보았다. 주사된 아메바에서는 공생낭과 리소솜간의 융합이 일어나는 것으로 미루어 보아, 아마도 lipopolysaccharides는 융합저해 요소 중의 하나로 사료되어 진다.

• Mycobiology
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• 제43권4호
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• pp.450-457
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• 2015

Medicinal mushrooms have been used worldwide to treat cancer and modulate the immune system. Over the last several years, there has been increasing interest in isolating bioactive compounds from medicinal mushrooms and evaluating their health beneficial effects. Fomes fomentarius is used in traditional oriental medicine and is known to possess antioxidant, antiinflammatory, antidiabetic, and antitumor effects. In the present study, we isolated fomentariol from Fomes fomentarius and investigated its anti-inflammatory effect in murine macrophages (RAW264.7 cells) stimulated with lipopolysaccharides. Fomentariol inhibited the production of nitric oxide and intracellular reactive oxygen species triggered by lipopolysaccharides. Interestingly, fomentariol differentially regulated cytokine production triggered by lipopolysaccharides. Fomentariol effectively suppressed the production of interleukin-$1{\beta}$ and interleukin-6 but not tumor necrosis factor-${\alpha}$. The inhibitory effect of fomentariol against nitric oxide, interleukin-$1{\beta}$, and interleukin-6 production was possibly mediated by downregulation of the extracellular signal-regulated kinase signaling pathway. Taken together, our results suggest that fomentariol differentially modulated inflammatory responses triggered by lipopolysaccharides in macrophages and is one of the bioactive compounds that mediate the physiological effects of Fomes fomentarius.

• International Journal of Oral Biology
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• 제44권4호
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• pp.160-164
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• 2019

Porphyromonas gingivalis (Pg), Aggregatibacter actinomycetemcomitans (Aa), Tannerella forsythia (Tf), Prevotella intermedia (Pi), and Fusobacterium nucleatum (Fn) are major periodontal pathogens. Lipopolysaccharides (LPSs) from periodontal bacteria play an important role in periodontal pathogenesis by stimulating host cells to produce inflammatory cytokines. In this study, highly pure LPSs from the five major periodontopathogens were prepared, and their monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-α (TNF-α)-inducing activities were compared in human umbilical vein endothelial cells (HUVECs) and THP-1 macrophagic cells, respectively. In HUVECs, LPSs from Aa and Fn were potent stimulators for MCP-1 induction; however, LPSs from Pg, Pi, and Tf were much weaker MCP-1 inducers. In THP-1 cells, LPSs from Pg, Aa, and Fn were relatively strong inducers of TNF-α, whereas LPSs from Pi and Tf produced little activity. The Toll-like receptor (TLR)2/TLR4 dependency of various LPSs was also determined by measuring NF-κB reporter activity in TLR2- or TLR4-expressing 293 cells. LPSs from Aa, Fn, and Tf stimulated only TLR4; however, LPSs from Pg and Pi stimulated both TLR2 and TLR4. These results suggest that LPSs from major periodontal bacteria differ considerably in their cell-stimulating activity.

• Biomolecules & Therapeutics
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• 제20권6호
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• pp.556-561
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• 2012

Steroid sulfatase (STS) is responsible for the conversion of estrone sulfate to estrone that can stimulate growth in endocrine-dependent tumors such as prostate cancer. Although STS is considered as a therapeutic target for the estrogen-dependent diseases, cellular function of STS are still not clear. Previously, we found that tumor necrosis factor (TNF)-${\alpha}$ significantly enhances steroid sulfatase expression in PC-3 human prostate cancer cells through PI3K/Akt-dependent pathways. Here, we studied whether bacterial lipopolysaccharides (LPS) which are known to induce TNF-${\alpha}$ may increase STS expression. Treatment with LPS in PC-3 cells induced STS mRNA and protein in concentration- and time-dependent manners. Using luciferase reporter assay, we found that LPS enhanced STS promoter activity. Moreover, STS expression induced by LPS increased PC-3 tumor cell migration determined by wound healing assay. We investigated that LPS induced IL-6 expression and IL-6 increased STS expression. Taken together, these data strongly suggest that LPS induces STS expression through IL-6 pathway in human prostate cancer cells.

• 대한수의학회지
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• 제40권1호
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• pp.72-80
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• 2000

Lipopolysaccharides (LPS) of Pasteurella multocida (P multocida) and several Gram-negative bacterial pathogens were analyzed by methanolysis, trifluoroacetylation and gas chromatography (GC) on a fused-silica capillary column. The GC analysis indicated that LPS prepared from a strain of P multocida by phenol-water (PW) or trichloroacetic acid (TCA) extraction were quite different in chemical composition. However, LPS prepared from Salmonella enteritidis by the two extraction methods were very similar. PW-LPS extracts from different Pasteurella strains of a serotype had essentially identical GC patterns. Endotoxic LPS extracted from 16 different serotypes of P multocida by PW or by phenol-chloroform-petroleum ether procedures yielded chromatograms indicating similar composition of the fatty acid moieties but minor differences in carbohydrate content. When the chemical composition of endotoxic LPS extracted from several Gram-negative bacteria (P multocida, Pasteurella hacmolytica, Haemophilus somnus, Actinobacillus ligniersii, Brucella abortus, Treponema hyodysenteriae, Escherichia coli, Bacteriodes fragilis, Salmonella abortus equi and Salmonella enteritidis) were examined, each bacteria showed a unique GC pattern. The carbohydrate constituents in LPS of various Gram-negative bacteria were quite variable not only in the O-specific polysaccharides but also in the core polysaccharides. The LPS of closely related bacteria shared more fatty acid constituents with each other than with unrelated bacteria.

• Journal of Periodontal and Implant Science
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• 제24권1호
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• pp.98-108
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• 1994

Gingival hyperplasia is frequently associated with the long-term use of phenytoin for control of convulsive disorder. The purpose of this study was to investigate on the effects of lipopolysaccharides (LPS), ursolic acid and oleanolic acid to phenytoin-induced cell activity in human gingival fibroblast. Human gingival fibroblasts were cultured form the healthy gingiva of orthodontic patients. Gingival fibroblasts were trypsinized and transferred to the weels of microtest plates. Fibroblast were cultured in growth medium added $5{\mu}g/ml$ of phenytoin, $5{\mu}g/ml$ of LPS, $10^{-7}M$ of ursolic acid and oleanolic acid. The passage number of cultured fibroblasts were fifth and eight. Cell morphology was examined by inverted microscope and the cell activity was measured by proliferation assay. Ursolic acid significantly modulated cell morphology into globular shape at the concentrantion of $10^{-7}M$ in the presence of phenytoin and LPS, and the cell activity was significantl decreased by ursolic acid or oleanolic acid regardless of the presence of phenytoin and LPS. These results suggested that the increased phenytoin-induced cell activity might be modulated by ursolic acid regardless of the presence of phenytoin and LPS. These results suggested that the increased phenytoin-induced cell activity might be modulated by ursolic acid or oleanolic acid. Further study is needed to clarify their toxicological effects on cellular modulation and mRNA expression change.

• 한국수산과학회지
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• 제52권1호
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• pp.81-86
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• 2019

The common hallmark of several neurodegenerative disorders, including Alzheimer's disease (AD), is the presence of chronic neuroinflammation, which contributes to the loss of neuronal structure and function. This study investigated the effects of an ethanolic extract of Sargassum serratifolium (SSE) in a lipopolysaccharides (LPS)-induced murine neuroinflammation model. Mice were administered SSE (100 mg/kg body weight) or vehicle for 5 days by oral gavage, and then treated with LPS or saline by intraperitoneal injection. Thereafter, the brain tissues were collected, and the expression of pro-inflammatory cytokines was analyzed by quantitative real-time RT-PCR. There was a marked increase in the spleen weight index in the LPS-treated groups, which indicated the induction of acute systemic inflammation. Based on significant increases in the levels of IL-1 and IL-6 expression, the induction of neuroinflammation was also evident in the cortex and hippocampus of the LPS-treated groups. The overall expression of IL-1 and IL-6 was decreased slightly by SSE administration, compared with the LPS group, and a marked change in IL-1 was observed in the cortex of the SSE-treated (SSE/LPS) group. These results suggest that SSE has potential as an anti-neuroinflammatory nutraceutical.

• 농업과학연구
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• 제48권1호
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• pp.163-170
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• 2021

Bacterial infections in the female reproductive tract negatively affect ovarian function, follicular development, and embryo development, leading to the eventual failure of fertilization. Moreover, bacterial lipopolysaccharides (LPS) can interfere with the immune system and reproductive system of the host animal. Therefore, this study examined the effect of LPS on the in vitro maturation (IVM) of pig oocytes. Oocytes were matured in TCM199 medium in the presence of varying concentrations of LPS (0 - 50 ㎍·mL^-1). The maturation rate, cortical granules (CGs) migration, and chromosome alignment were subsequently evaluated during the meiotic development of the oocytes. We observed a dose-dependent and significant decrease in the metaphase II (MII) rate with increasing concentrations of LPS (97.6% control [0 ㎍·mL^-1 LPS] vs. 10.4-74.9% LPS [1 - 50 ㎍·mL^-1], p < 0.05). In addition, compared to the control oocytes without LPS, higher levels of abnormal CGs distribution (18.1 - 50.0% LPS vs. 0% control), chromosome/spindle alignment (20.3 - 56.7% LPS vs. 0% control), and intracellular ROS generation were observed in oocytes matured with LPS (p < 0.05). Nitrite levels were also increased in the maturation medium derived from the oocytes matured with LPS (p < 0.05). These results indicate that LPS induces oxidative stress during IVM and affects oocyte maturation, including CGs migration and chromosome alignment of pig oocytes.

• Biomolecules & Therapeutics
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• 제31권1호
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• pp.27-39
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• 2023

Extensive research supported the therapeutic potential of curcumin, a naturally occurring compound, as a promising cytokine-suppressive anti-inflammatory drug. This study aimed to investigate the synergistic anti-inflammatory and anti-cytokine activities by combining 6-shogaol and 10-shogaol to curcumin, and associated mechanisms in modulating lipopolysaccharides and interferon-γ-induced proinflammatory signaling pathways. Our results showed that the combination of 6-shogaol-10-shogaolcurcumin synergistically reduced the production of nitric oxide, inducible nitric oxide synthase, tumor necrosis factor and interlukin-6 in lipopolysaccharides and interferon-γ-induced RAW 264.7 and THP-1 cells assessed by the combination index model. 6-shogaol-10-shogaol-curcumin also showed greater inhibition of cytokine profiling compared to that of 6-shogaol-10-shogaol or curcumin alone. The synergistic anti-inflammatory activity was associated with supressed NFκB translocation and downregulated TLR4-TRAF6-MAPK signaling pathway. In addition, SC also inhibited microRNA-155 expression which may be relevant to the inhibited NFκB translocation. Although 6-shogaol-10-shogaol-curcumin synergistically increased Nrf2 activity, the anti-inflammatory mechanism appeared to be independent from the induction of Nrf2. 6-shogaol-10-shogaol-curcumin provides a more potent therapeutic agent than curcumin alone in synergistically inhibiting lipopolysaccharides and interferon-γ induced proinflammatory mediators and cytokine array in macrophages. The action was mediated by the downregulation of TLR4/TRAF6/MAPK pathway and NFκB translocation.

• Journal of Microbiology and Biotechnology
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• 제23권4호
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• pp.518-526
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• 2013

Gut-derived lipopolysaccharides (LPS) are critical to the development and progression of chronic low-grade inflammation and metabolic diseases. In this study, the effects of probiotics Lactobacillus and Bifidobacterium on gut-derived lipopolysaccharide and inflammatory cytokine concentrations were evaluated using a human colonic microbiota model. Lactobacillus reuteri, L. rhamnosus, L. plantarum, Bifidobacterium animalis, B. bifidum, B. longum, and B. longum subsp. infantis were identified from the literature for their anti-inflammatory potential. Each bacterial culture was administered daily to a human colonic microbiota model during 14 days. Colonic lipopolysaccharides, and Gram-positive and negative bacteria were quantified. RAW 264.7 macrophage cells were stimulated with supernatant from the human colonic microbiota model. Concentrations of TNF-${\alpha}$, IL-$1{\beta}$, and IL-4 cytokines were measured. Lipopolysaccharide concentrations were significantly reduced with the administration of B. bifidum ($-46.45{\pm}5.65%$), L. rhamnosus ($-30.40{\pm}5.08%$), B. longum ($-42.50{\pm}1.28%$), and B. longum subsp. infantis ($-68.85{\pm}5.32%$) (p < 0.05). Cell counts of Gram-negative and positive bacteria were distinctly affected by the probiotic administered. There was a probiotic strain-specific effect on immunomodulatory responses of RAW 264.7 macrophage cells. B. longum subsp. infantis demonstrated higher capacities to reduce TNF-${\alpha}$ concentrations ($-69.41{\pm}2.78%$; p < 0.05) and to increase IL-4 concentrations ($+16.50{\pm}0.59%$; p < 0.05). Colonic lipopolysaccharides were significantly correlated with TNF-${\alpha}$ and IL-$1{\beta}$ concentrations (p < 0.05). These findings suggest that specific probiotic bacteria, such as B. longum subsp. infantis, might decrease colonic lipopolysaccharide concentrations, which might reduce the proinflammatory tone. This study has noteworthy applications in the field of biotherapeutics for the prevention and/or treatment of inflammatory and metabolic diseases.