• Proceedings of the PSK Conference
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• 2003.10b
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• pp.132.2-132.2
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• 2003

Vibrio vulnificus, a Gram-negative estuarine bacterium, is the causative agent of food-borne diseases, such as life-threatening septicemia. V. vulnificus penetrating into the intestinal epithelial barrier stimulates an inflammatory response in the adjacent intestinal mucosa. Therefore, interaction between V. vulnificus and intestinal cells is important for understanding of both the immunology of mucosal surfaces and V. vulnificus. In this study we investigated the effects of V. vulnificus infection on cytokine gene expression of human intestinal epithelial cells, Caco-2 and INT-407 cells. (omitted)

• The Journal of Korean Medicine
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• v.23 no.3
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• pp.200-210
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• 2002

Objectives: Dojeckjiyu-tang has been used to treat Hwaseol & Jeokri. The object of this study is examination of the treatment effect of Dojeckjiyu-tang for ulcerative colitis of the mouse descending colon. Methods and Materials : Twenty-one rats were divided into 3 groups and treated as follows: the control group was untreated mice. The UCE group was ulcerative colitis elicited mice. The DJT group was Dojeckjiyu-tang treated mice after ulcerative colitis elicitation. The groups were examined with common morphology, paneth cells in intestinal crypt, absorptive cells and goblet cells in epithelium, cell division in mucose, COX-1 as mucosal protector, COX-2 (which appears to play an important role in inflammation), IL-2R-, ICMA-1-inducing cellular immuno-chainreaction, and the distribution of apoptotic cells. Results: 1. The morphology of colonic mucosa from UCE mice: the disappearance of epithelium and intestinal propria in hemorrhagic erosions were seen, but in the morphology of colonic mucosa from DJT-treated mice, the configuration of epithelium and intestinal propria were the same as normal. 2. The distribution of goblet cells and absorptive cells with microvilli in intestinal propria from UCE mice: a noticeable decrease of goblet cells and absorptive cells with microvilli were seen, but with the distribution of goblet cells and absorptive cells with microvilli in intestinal propria from DJT -treated mice, the configuration of goblet cells and absorptive cells with microvilli were the same as normal. 3. The immunohistochemical stain for BrdD in colonic mucosa and COX-1 in lamina propria from UCE mice: BrdU positive cells and COX-1 positive cells in the region of hemorrhagic erosion disappeared, but in the immunohistochemical stain for BrdU in colonic mucosa and COX-1 in lamina propria from DIT-treated mice, BrdU positive cells and COX-1 positive cells were seen. 4. The immunohistochemical stain for COX-2 in lamina propria, IL-2R-in lamina propria, intestinal propria and submucosa and ICMA-1 in intestinal propria and submucosa from DCE mice: a noticeable increase COX-2, IL-2R-, ICMA-1 positive cells were seen, but in the immunohistochemical stain for COX-2 in lamina propria, IL-2R-in lamina propria, intestinal propria and submucosa and ICMA-1 in intestinal propria and submucosa from DJT-treated mice, a numerical decrease of COX-2, IL-2R-, ICMA-1 positive cells was observed. 5. The distribution of apoptotic cells in epithelium and lamina propria from UCE mice: a noticeable increase of apoptotic cells in region of hemorrhagic erosion was seen, but in the distribution of apoptotic cells in epithelium and lamina propria from DJT-treated mice, a remarkable decrease of apoptotic cells was seen. Conclusions: According to the above results, Dojeckjiyu-tang has a moderate effect on ulcerative colitis in descending colon.

• IMMUNE NETWORK
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• v.15 no.1
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• pp.1-8
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• 2015

Innate immune cells survey antigenic materials beneath our body surfaces and provide a front-line response to internal and external danger signals. Dendritic cells (DCs), a subset of innate immune cells, are critical sentinels that perform multiple roles in immune responses, from acting as principal modulators to priming an adaptive immune response through antigen-specific signaling. In the gut, DCs meet exogenous, non-harmful food antigens as well as vast commensal microbes under steady-state conditions. In other instances, they must combat pathogenic microbes to prevent infections. In this review, we focus on the function of intestinal DCs in maintaining intestinal immune homeostasis. Specifically, we describe how intestinal DCs affect IgA production from B cells and influence the generation of unique subsets of T cell.

• Journal of Microbiology and Biotechnology
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• v.14 no.2
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• pp.350-355
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• 2004

Sulforhodamine B (SRB) assay is a rapid, sensitive, and inexpensive method for measuring cell proliferation and chemosensitivity. However, the lactate dehydrogenase (LDH) release assay is generally used to measure cytototoxicity of infectious microorganisms against host cells. In this study, we investigated the possibility of applying the SRB assay to determine cytotoxicity for infectious microorganisms, and compared the results with those obtained by the LDH release assay. We used Vibrio vulnificus as a model of infectious microorganisms. The SRB assay showed that V vulnificus strongly induced cytotoxic activity against human intestinal cells, Caco-2 and INT-407 cells. The degree of cytotoxicity closely correlated with infection time and number ratios of V. vulnificus to intestinal cells (MOI, multiplicity of infection). Furthermore, cytotoxicity values obtained by SRB assay correlated well with results obtained by the LDH release assay, and both assays gave a linear response with respect to MOI Heat-inactivation of V. vulnificus for 35 min at $60^{\circ}C$ did not induce cytotoxic activity, indicating that viability of V. vulnificus is crucial for cytotoxic activity against intestinal cells. Although both assays are suitable as cytotoxicity endpoints, the SRB assay is recommended for measuring cytotoxicity of infectious microorganisms against host cells because of its significantly lower cost and more stable endpoint than the LDH release assay.

• Journal of Microbiology and Biotechnology
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• v.31 no.8
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• pp.1175-1182
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• 2021

We investigated the effect of bovine lactoferricin (Lfcin-B), a peptide derived from bovine lactoferrin, on activation of intestinal epithelial cells in IEC-6 intestinal cell, and protection against in vivo rotavirus (RV) infection. Treatment with Lfcin-B significantly enhanced the growth of IEC-6 cells and increased their capacity for attachment and spreading in culture plates. Also, Lfcin-B synergistically augmented the binding of IEC-6 cells to laminin, a component of the extracellular matrix (ECM). In the analysis of the intracellular mechanism related to Lfcin-B-induced activation of IEC-6 cells, this peptide upregulated tyrosine-dependent phosphorylation of focal adhesion kinase (FAK) and paxillin, which are intracellular proteins associated with cell adhesion, spreading, and signal transduction during cell activation. An experiment using synthetic peptides with various sequences of amino acids revealed that a sequence of 9 amino acids (FKCRRWQWR) corresponding to 17-25 of the N-terminus of Lfcin-B is responsible for the epithelial cell activation. In an in vivo experiment, treatment with Lfcin-B one day before RV infection effectively prevented RV-induced diarrhea and significantly reduced RV titers in the bowels of infected mice. These results suggest that Lfcin-B plays meaningful roles in the maintenance and repair of intestinal mucosal tissues, as well as in protecting against intestinal infection by RV. Collectively, Lfcin-B is a promising candidate with potential applications in drugs or functional foods beneficial for intestinal health and mucosal immunity.

• International Journal of Industrial Entomology and Biomaterials
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• v.43 no.2
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• pp.94-98
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• 2021

Reactive oxygen species (ROS) induce a variety of cellular responses, such as proliferation, differentiation, senescence, and apoptosis. Intestinal epithelial cells are continuously exposed to ROS, and excessive generation of ROS severely damages cells via oxidative stress. Pro-inflammatory cytokines may lead to intestinal inflammation and damage by inducing excessive ROS generation. In this study, we showed that papiliocin, an antimicrobial peptide, significantly inhibited ROS production, without affecting cell viability. Moreover, TNF-α and IL-6 expression was decreased in the intestinal epithelial cells. The activity of papiliocin may significantly contribute to preserving the integrity of the intestinal mucosa against oxidative damage and inflammation-related disorders.

• Journal of Nutrition and Health
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• v.34 no.2
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• pp.150-157
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• 2001

Intestinal absorption of dietary taurine is one of the regulatory component maintaining taurine homeostasis along with renal reabsorption, bile acid conjugation and secretion, and de nobo synthesis of taurine in mammals. Recent observations of decreased enterocytic levels of taurine in response to trauma, infection and surgical insults, postulate the possibility that intestinal taurine absorption might be impaired in such stressed conditions. The aim of the present study was to evaluate changes in enterocytic taurine transporter activity using the human intestinal colon carcinoma cell line, HT-29, in various stress-induced conditions. Pretreatment of the HT-29 cells with dexamethasone, a stress hormone(0.1,1,10 or 100$\mu$M) for 3 hrs, or with E coli heat-stable enterotoxin(10, 100, or 200nM) for 30 minutes in order to induce the condition of enterotoxigenic infection did not influence taurine uptake as compared to the value found in control cells. In contrast, pretreatment of the cells with cholera toxin(10, 100, 500, or 1000ng/ml)for 3hr or 24hr significantly decreased taurine uptake by HT-29 cells to 40~50% of the value found in untreated control cells. Kinetic studies of the taurine transporter activity were conducted in control and cholera toxin treated HT-29 cells with varying taurine concentrations(2~60$\mu$M) in the uptake medium. Pretreatment of the cells with cholera toxin(100ng/ml) for 3hr did not influence the Vmax, but resulted in a 55% increase in the Michaelis-Menten constant(Km) of the taurine transporter compared to those in control cells. These results suggest that cholera toxin-induced reduction in taurine transporter activity in HT-29 cells is associated with decreased affinity of the taurine transporter without altering the amount of transporter protein. Intestinal taurine absorption appears to be reduced in the condition of water-borne diseases caused by bacteria such as V. cholerae. This might influence the taurine status of infants and young children more readily, an age group in which the prevalence of intestinal infection is high and the role of intestinal absorption is crucial for maintaining the body taurine pool. (Korean J Nutrition 34(2) : 150-157, 2001)

• Journal of Environmental Science International
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• v.28 no.2
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• pp.249-257
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• 2019

Ulmus davidiana Nakai (UDN) has been traditionally used as a herbal medicine to treat inflammatory diseases in Korea. In the present study, we investigated the anti-ecotoxic potential of a 116 kDa glycoprotein isolated from UDN (UDN glycoprotein) in human intestinal epithelial INT-407 cells. We demonstrated that UDN glycoprotein ($20{\mu}g/mL$) could inhibit the production of lactate dehydrogenase (LDH) induced by toluene, an ecotoxic substance. Additionally, we found that the toluene-induced intestinal cytotoxicity was mediated by the phosphorylation of p38 Mitogen-Activated Protein Kinase (MAPK) via the production of intracellular Reactive Oxygen Species (ROS). The UDN glycoprotein significantly decreased the levels of ROS production and p38 MAPK activation in toluene-stimulated INT-407 cells. Moreover, the UDN glycoprotein inhibits the phosphorylation of nuclear factor-kappa B ($NF-{\kappa}B$), which is responsible for the production of LDH, in toluene-stimulated INT-407 cells. Collectively, our data indicate that UDN glycoprotein is a natural antioxidant and a modulator of ecotoxicity signaling pathways in human intestinal epithelial cells.

• The Journal of the Korean Society for Microbiology
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• v.34 no.5
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• pp.479-489
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• 1999

Invasion of enteric bacteria, such as Salmonella and invasive E. coli, into intestinal epithelial cells induces proinflammatory gene responses and finally epithelial cell apoptosis. In this study, we asked whether invasive bacterial infection of human intestinal epithelial cells could upregulate cyclooxygenase-2 (COX-2) gene expression and whether increased COX-2 expression could influence intestinal epithelial cell apoptosis. Expression of COX-2 mRNA and prostaglandin (PG) $E_2$ production were upregulated in HT-29 colon epithelial cells which were infected with S. dublin or invasive E. coli, as examined by quantitative RT-PCR and radioimmunoassay. Inhibition of COX-2 expression and $PGE_2$ production using NS-398, a specific COX-2 inhibitor, showed a significant increase of epithelial cell apoptosis and caspase-3 activation in HT-29 cells infected with invasive bacteria. However, the addition of valerylsalicylate, a specific COX-1 inhibitor, did not change apoptosis in S. dublin-infected HT-29 cells. These results suggest that up regulated COX-2 expression and $PGE_2$ production in response to invasive bacterial infection could contribute to host defense by inhibiting apoptosis of intestinal epithelial cells.

• Journal of Microbiology and Biotechnology
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• v.25 no.4
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• pp.479-491
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• 2015

Lactobacillus species have been shown to enhance intestinal epithelial barrier function, modulate host immune responses, and suppress the growth of pathogenic bacteria, yeasts, molds, and viruses. Thus, lactobacilli have been used as probiotics for treating various diseases, including intestinal disorders, and as biological preservatives in the food and agricultural industries. However, the molecular mechanisms used by lactobacilli to suppress pathogenic bacterial infections have been poorly characterized. We previously isolated Lactobacillus plantarum JSA22 from buckwheat sokseongjang, a traditional Korean fermented soybean food, which possessed high enzymatic, fibrinolytic, and broad-spectrum antimicrobial activity against foodborne pathogens. In this study, we investigated the effects of L. plantarum JSA22 on the growth of S. Typhimurium and S. Typhimurium-induced cytotoxicity by stimulating the host immune response in intestinal epithelial cells. The results showed that coincubation of S. Typhimurium and L. plantarum JSA22 with intestinal epithelial cells suppressed S. Typhimurium infection, S. Typhimurium-induced NF-κB activation, and IL-8 production, and lowered the phosphorylation of both Akt and p38. These data indicated that L. plantarum JSA22 has probiotic properties, and can inhibit S. Typhimurium infection of intestinal epithelial cells. Our findings can be used to develop therapeutic and prophylactic agents against pathogenic bacteria.