• Korean Journal of Agricultural Science
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• v.48 no.1
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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.

• Proceedings of the Korea Society of Poultry Science Conference
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• 2002.11a
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• pp.94-95
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• 2002

In order to evaluate the effect of dietary krill meal on immunity of broilers, the proliferation of splenocyte and PBMC (pheripheral blood mononuclear cell) from broilers fed experimental diets containing 0.0, 0.5, 1.0 and 2.0 o/o krill meal, respectively, and injected the Salmonella typhymurium lipopolysaccharide (LPS) were assayed. The proliferation of splenocyte was increased with the dietary krill levels, but was decreased with the LPS immunlogical stress. Con A addition in the medium increased the proliferation of the splenocytes from birds fed dietary krill or stimulated by LPS. In 21 day old broilers, dietary krill meal and addition of Con A decreased the proliferation of PBMC while enhanced proliferation of PBMC was shown in birds stressed by the LPS during 2nd week of age. The results indicated dietary krill meal affected immune response in broiler.

• Journal of Microbiology and Biotechnology
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• v.28 no.3
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• pp.491-497
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• 2018

Lipopolysaccharide (LPS), a component of the cell wall of gram-negative bacteria, elicits the secretion of cytokines, such as interferons, that stimulate the host defense system. Previously, we demonstrated that interferons induce interferon regulatory factors (IRFs) 1, 3, and 7, which regulate the transcription of Noxa and alter the expression profiles of Bcl-2 family proteins in tumors. However, the immediate consequences of LPS stimulation on Noxa and BH3 expression in tumor cells remain uncharacterized. In this study, we determined that LPS induced Noxa expression in CT26 cells. Furthermore, studies in HCT116 parental and HCT116 p53-deficient cells revealed that LPS-mediated Noxa was independent of p53. Meanwhile, IRF1, 3, and 7 in CT26, HCT116 parental, and HT116 p53-deficient cells were upregulated by LPS stimulation, suggesting that LPS induces the expression of these IRFs in a p53-independent manner. The responsiveness of IRF1, 3, 4, and 7 binding to the Noxa promoter region to LPS indicated that IRF1, 3, and 7 activated Noxa expression, whereas IRF4 repressed Noxa expression. Together, these results suggest that LPS directly affects Noxa expression in tumor cells through IRFs, implicating that it may contribute to LPS-induced tumor regression.

• YAKHAK HOEJI
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• v.45 no.5
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• pp.557-564
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• 2001

To determine effects of zinc on lipopolysaccharide (LPS)-induced production of proinflammatory cytokines and Iymphokines in tumor-bearing ICR mice, this study has been investigated. Zinc chloride (Zn) at doses of 1 mg/kg was administered orally 30 minutes before i.p. injection of LPS (8 mg/kg) 5 times for 7 days. LPS greatly increased tumor necrosis factor (TNF)-$\alpha$ and interleukin (IL)-1$\beta$, in both serum and splenic supernatants compared with those in controls. However Zn strongly decreased LPS-increased production of TNF-$\alpha$ and IL-1$\beta$ in spleenic supernatants compared with those in controls and insignificantly also reduced in serum. LPS insignificantly decreased IL-2 levels in spleenic supernatants compared with those in controls but significantly increased interferon (IFN)-${\gamma}$ levels. Zn didn't affect IL-2 production in splenic supernatants compared to controls but significantly enhanced the LPS-decreased production of IL-2. Zn significantly increased IFN-${\gamma}$ levels in splenic supernatants compared to controls and did not affect the LPS-increased production of IFN-${\gamma}$. These findings suggest that Zn may strongly attenuate the LPS-induced pathogenesis of proinflammatory cytokines in tumor-bearing state and significantly up-regulate the LPS-induced function of T cells to produce IL-2 with maintaining normally the LPS- increased levels of IFN-${\gamma}$.

• Journal of Microbiology and Biotechnology
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• v.33 no.8
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• pp.998-1005
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• 2023

Streptococcus salivarius is a beneficial bacterium in oral cavity, and some strains of this bacterium are known to be probiotics. The purpose of this study was to investigate the anti-inflammatory effect and mechanism of S. salivarius G7 lipoteichoic acid (LTA) on lipopolysaccharide (LPS) and LTA of periodontopathogens. The surface molecules of S. salivarius G7 was extracted, and single- or co-treated on human monocytic cells with LPS and LTA of periodontopathogens. The induction of cytokine expression was evaluated by real-time PCR and ELISA. After labeling fluorescence on LPS and LTA of periodontopathogens, it was co-treated with S. salivarius LTA to the cell. The bound LPS and LTA were measured by a flow cytometer. Also, the biding assay of the LPS and LTA to CD14 and LPS binding protein (LBP) was performed. The surface molecules of S. salivarius G7 did not induce the expression of inflammatory cytokines, and S. salivarius G7 LTA inhibited the inflammatory cytokines induced by LPS and LTA of periodontopathogens. S. salivarius G7 LTA inhibited the binding of its LPS and LTA to cells. Also, S. salivarius G7 LTA blocked the binding of its LPS and LTA to CD14 and LBP. S. salivarius G7 has an inhibitory effect on inflammation induced by LPS or LTA of periodontopathogens, and may be a candidate probiotics for prevention of periodontitis.

• Tuberculosis and Respiratory Diseases
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• v.49 no.6
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• pp.691-702
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• 2000

Background : Acute lung injury (ALI) is a commonly encountered respiratory disease and its prognosis is poor when the treatment is not provided promptly and properly. However no specific pharmacologic treatment is currently available for ALI, although recently several supportive drugs have been under scrutiny. We studied anti-inflammatory effects of pentoxifylline (PF), a methylated xanthine, and ONO-5046, a synthetic neutrophil elastase inhibitor on lipopolysaccharide (LPS)-induced ALI in vitro. Methods : To establish an in vitro model of LPS-induced ALI, primary rat alveolar macrophages and peripheral neutrophils in various ratios (1:0, 5:1, 1:1, 1:5, 0:1) were co-cultured with transformed rat alveolar epithelial cells (L2 cell line) or vascular endothelial cells (IP2-E4 cell line) under LPS stimulation. Each experiment was divided into five groups-control, LPS, LPS+PF, LPS+ONO, and LPS+PF+ONO. We compared LPS-induced superoxide anion productions from primary rat alveolar macrophages and peripheral neutrophils in various ratios, and the resultant cytotoxicity on L2 cells or IP2-E4 cells between groups. In addition we also compared the productions of tumor necrosis factor (TNF)-$\alpha$ interleukin (IL)-$1{\beta}$, monocyte chemotactic protein(MCP)-1, IL-6, and IL-10 as well as mRNA expressions of TNF-$\alpha$ inducible nitric oxide synthetase(iNOS), and MCP-1 from LPS-stimulated primary rat alveolar macrophages between groups. Results : (1) PF and ONO-5046 in each or both showed a trend to suppress LPS-induced superoxide anion productions from primary rat alveolar macrophages and peripheral neutrophils regardless of their ratio, except for the LPS+PF+ONO group with the 1:5 ratio, although statistical significance was limited to a few selected experimental conditions. (2) PF and ONO-5046 in each or both showed a trend to prevent IP2-E4 cells from LPS-induced cytotoxicity by primary rat alveolar macrophages and peripheral neutrophils regardless their ratio, although statistical significance was limited to a few selected experimental conditions. the effects of PF and/or ONO-5046 on LPS-induced L2 cell cytotoxicity varied according to experimental conditions. (3) PF showed a trend to inhibit LPS-induced productions of INF-$\alpha$ MCP-1, and IL-10 from primary rat alveolar macrophages. ONO-5046 alone didnot affect the LPS-induced productions of proinflammatory cytokines from primary rat alveolar macrophages but the combination of PF and ONO-5046 showed a trend to suppress LPS-induced productions of INF-$\alpha$ and IL-10 PF and ONO-5046 in each or both showed a trend to increase LPS-induced IL-$\beta$ and IL-6 productions from primary rat alveolar macrophages. (4) PF and ONO-5046 in each or both showed a trend to attenuate LPS-induced mRNA expressions of TNF-$\alpha$ and MCP-1 from primary rat alveolar macrophages but at the same time showed a trend increase iNOS mRNA expression. Conclusion : These results suggest that PF and ONO-5046 may play a role in attenuating inflammation in LPS-induced ALI and that further study is needed to use these drugs as a new supportive therapeutic strategy for ALI.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1994.04a
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• pp.318-318
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• 1994

Addition of AAF to murine splenocytes culture produced a dose-related suppression of lymphoproliferative response to lipopolysaccharide (LPS). The time course of the suppression showed that a significant inhibition was occured after a 18 hr AAF treatment. Total protein kinase C activity in splenocytes was decreased to 72% of control level after a 18 hr AAF treatment. Phosphorylation of a PKC specific 80 kDa protein was increased by LPS and AAF down-regulated LPS-induced PKC activity. LPS-induced phosphorylation of overall proteins in membrane and cytosolic fraction were also decreased by the treatment of AAF. A significant increase of PKC activity in membrane fraction was noticed within 10 min of AAF treatment compared to LPS alone and then gradually decreased to LPS level in 60 min. Meanwhile, PKC activity in cytosolic fraction was increased slightly in 10 min by the treatment of AAF and then decrease to 80% LPS level in 30 min. These results suggested that suppressive effect of AAF on LPS-induced lymphoproliferative response may be associated with the down-regulation of PKC and other susceptible kinases in spleen cells.

• YAKHAK HOEJI
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• v.52 no.1
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• pp.43-47
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• 2008

To determine the regulatory roles of PDE4 inhibitor on LPS-induced osteoclastogenesis, we investigated the effect of a PDE4 inhibitor on osteoclast formation in the presence of LPS. A specific PDE4 inhibitor, rolipram, increased LPS-induced osteoclast formation in cocultures. To verify that whether rolipram acts indirectly on osteoblasts, we investigated the TRANCE and COX-2 mRNA expression levels in osteoblasts. Treatment of rolipram increased the expression of TRANCE and COX-2 mRNA in osteoblasts stimulated by LPS. On the contrary, rolipram did not augment the number of osteoclasts differentiated from bone marrow cells by LPS. In conclusion, the stimulation of LPS-induced osteoclast formation by the PDE4 inhibitor are attributable to its indirect effect on osteoblasts, not to their direct effect on bone marrow-derived osteoclast precursors.

• Journal of Food Hygiene and Safety
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• v.11 no.4
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• pp.227-234
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• 1996

This study was designed to characterize endotoxin-induced prostaglandin production in primary cultured rat vascular smooth muscle cells (VSMC). The time course for prostaglandin synthesis in lipopolysaccharide (LPS)-stimulated VSMC showed that the maximum production was reached in 12 hours. LPS induced prostaglandin H2 synthase (PGHS) activity in VSMC and the time course profile in the changes of PGHS activity paralleled that of total prostaglandin production. Differential treatment showed that 4 hours' exposure to LPS was enough for the maximum effect on the prostaglandin production and this effect was completely inhibited by the co-treatment of actinomycin D, a transcription inhibitor. These results suggest that LPS effect might be determined within 4 hours. Actinomycin D increased PGHS activity without affecting prostaglandin production if added 4 hours after LPS treatment. On the other hand, cyclogeximide, a translation inhibitor, augmented LPS-induced prostaglandin production if treated during first four hours, but it inhibited LPS-induced PGHS activity regardless of treatment schedule. These results suggest the existence of multiple regulating mechanisms in the LPS-induced prostaglandin synthesis.

• YAKHAK HOEJI
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• v.53 no.4
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• pp.179-183
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• 2009

We explored the role of reactive oxygen species (ROS) in LPS-induced bone loss. LPS was shown to increase the concentration of ROS in osteoclast precursors. The antioxidant decreased osteoclast formation by LPS. Furthermore, the antioxidant decreased NFATc1 expression by LPS, suggesting that ROS mediates NFATc1 expression in the regulation of LPS-induced osteoclast formation. Finally, the antioxidant decreased LPS-induced RANKL mRNA expression in osteoblasts. Taken together, these data indicate that LPS mediates ROS to induce bone loss.