• Journal of Microbiology and Biotechnology
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• v.16 no.8
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• pp.1292-1300
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• 2006

Aeromonas encheleia, a potential human intestinal pathogen, was shown to infect a human intestinal epithelial cell line (Caco-2) in a noninvasive manner. The transcriptional profile of the Caco-2 cells after infection with the bacteria revealed an upregulated expression of genes involved in chloride secretion, including that of phospholipase A2 (PLA2) and platelet-activating factor (PAF) acetylhydrolase (PAFAH2). This was also confirmed by a real-time RT-PCR analysis. As expected from PLA2 induction, PAF was produced when the Caco-2 cells were infected with the bacteria, and PAF was also produced when the cells were treated with a bacterial culture supernatant including bacterial extracellular proteins, yet lacking lipopolysaccharides. Bacterial aerolysin was shown to induce the production of PAF.

• Parasites, Hosts and Diseases
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• v.55 no.6
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• pp.587-599
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• 2017

The immune response against Trichinella spiralis at the intestinal level depends on the $CD4^+$ T cells, which can both suppress or promote the inflammatory response through the synthesis of diverse cytokines. During the intestinal phase, the immune response is mixed (Th1/Th2) with the initial predominance of the Th1 response and the subsequent domination of Th2 response, which favor the development of intestinal pathology. In this context, the glucocorticoids (GC) are the pharmacotherapy for the intestinal inflammatory response in trichinellosis. However, its therapeutic use is limited, since studies have shown that treatment with GC suppresses the host immune system, favoring T. spiralis infection. In the search for novel pharmacological strategies that inhibit the Th1 immune response (proinflammatory) and assist the host against T. spiralis infection, recent studies showed that resiniferatoxin (RTX) had anti-inflammatory activity, which decreased the serum levels of IL-12, $INF-{\gamma}$, $IL-1{\beta}$, $TNF-{\alpha}$, NO, and $PGE_2$, as well the number of eosinophils in the blood, associated with decreased intestinal pathology and muscle parasite burden. These researches demonstrate that RTX is capable to inhibit the production of Th1 cytokines, contributing to the defense against T. spiralis infection, which places it as a new potential drug modulator of the immune response.

• 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 Applied Biological Chemistry
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• v.62 no.1
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• pp.101-107
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• 2019

The objectives of this study were to evaluate the anti-aging effects and investigate the effect of simulated gastrointestinal (GI) digestion on the anti-aging properties and intestinal permeation of the potential fish collagen hydrolysates (FCH). Therefore, procollagen synthesis, matrix metalloproteinase-1 (MMP-1) production, and Caco-2 cell permeability were analyzed before and after in vitro digestion for FCHs, low-molecular weight fractions (<1 kDa), and high molecular weight fractions (>1 kDa). After being subjected to GI digestion, the level of MMP-1 inhibition was maintained, although the procollagen production was significantly (>20%) lower with all samples. Also, the digested FCHs and their <1 kDa fraction yielded 9.1 and 13.8% increased peptide transport, respectively, compared to undigested samples. Based on the effective intestinal permeation and high digestive enzyme stability, the <1 kDa fraction of FCHs is a potential bioactive material suitable for anti-aging applications in the food and cosmetics industries.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.55 no.6
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• pp.960-966
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• 2022

We aimed to determine the dietary myo-inositol (MI) requirements of Pacific white shrimp Litopenaeus vannamei. A basal diet was formulated without myo-inositol (M0) and a negative control diet (M0-) was prepared by adding tetracycline hydrochloride to the basal diet to prevent intestinal inositol synthesis. Five MI diets were prepared by adding MI at 300, 600, 900, 1,200 and 1,500 mg/kg to the basal diet (designated as, M300, M600, M900, M1200 and M1500, respectively). Triplicate groups of shrimp (initial body weight, 0.55±0.01 g) were fed one of the experimental diets for 42 days. The growth performance of shrimp in M0- group was significantly lower when compared to that of shrimp in M0, M1200 and M1500 groups. Feed efficiency was significantly improved in M1200 and M1500 groups when compared to the M0 and M0- groups. GPx activity was significantly higher in M1200 and M1500 groups compared to that in M0 and M0- groups. Therefore, a practical diet (over 240 mg/kg) meets the minimum MI requirements of Pacific white shrimp. However, the optimum dietary MI level would be potentially above 1,200 mg/kg for better feed utilization efficiency and antioxidant capacity of Pacific white shrimp.

• Journal of Practical Agriculture & Fisheries Research
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• v.6 no.1
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• pp.90-101
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• 2004

Se is essential for a number of enzymes that perform important metabolic functions necessary for good health. However, people in many countries do not appear to consume adequate amounts of Se to support the maximal expression of the selenoproteins and Se retention in the body of animals and humans is dependent on the ingested Se source such as organic and inorganic Se. Therefore, this review was discussed to explore metabolic characterization regarding intestinal absorption, bioavailability and selenoprotein synthesis according to animal species such as monogastrics including human beings and ruminants. Generally, organic Se provided to animals is more effective than inorganic Se in body retention for the animal owing to the difference of manner for intestinal absorption. But, Se absorption in ruminants depending on its chemical form still remained questioned by several microbial actions and feeding regimen in the rumen. And Se absorbed through small intestine is utilized for the synthesis of selenoproteins and/or retained as selenoamino acids in the body. Retained Se in the body may be recycled to synthesize selenoproteins as lacked of dietary Se. In conclusion, desirable forms of Se ingestion in the animal may be useful for Se fortification in animal products as well as well being for humans and animals.

• Nutrition Research and Practice
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• v.10 no.5
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• pp.477-486
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• 2016

BACKGROUND/OBJECTIVES: Consumption of pine nut oil (PNO) was shown to reduce weight gain and attenuate hepatic steatosis in mice fed a high-fat diet (HFD). The aim of this study was to examine the effects of PNO on both intestinal and hepatic lipid metabolism in mice fed control or HFD. MATERIALS/METHODS: Five-week-old C57BL/6 mice were fed control diets containing 10% energy fat from either Soybean Oil (SBO) or PNO, or HFD containing 15% energy fat from lard and 30% energy fat from SBO or PNO for 12 weeks. Expression of genes related to intestinal fatty acid (FA) uptake and channeling (Cd36, Fatp4, Acsl5, Acbp), intestinal chylomicron synthesis (Mtp, ApoB48, ApoA4), hepatic lipid uptake and channeling (Lrp1, Fatp5, Acsl1, Acbp), hepatic triacylglycerol (TAG) lipolysis and FA oxidation (Atgl, Cpt1a, Acadl, Ehhadh, Acaa1), as well as very low-density lipoprotein (VLDL) assembly (ApoB100) were determined by real-time PCR. RESULTS: In intestine, significantly lower Cd36 mRNA expression (P<0.05) and a tendency of lower ApoA4 mRNA levels (P = 0.07) was observed in PNO-fed mice, indicating that PNO consumption may decrease intestinal FA uptake and chylomicron assembly. PNO consumption tended to result in higher hepatic mRNA levels of Atgl (P = 0.08) and Cpt1a (P = 0.05). Significantly higher hepatic mRNA levels of Acadl and ApoB100 were detected in mice fed PNO diet (P<0.05). These results suggest that PNO could increase hepatic TAG metabolism; mitochondrial fatty acid oxidation and VLDL assembly. CONCLUSIONS: PNO replacement in the diet might function in prevention of excessive lipid uptake by intestine and improve hepatic lipid metabolism in both control diet and HFD fed mice.

• Journal of Neurogastroenterology and Motility
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• v.24 no.4
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• pp.643-655
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• 2018

Background/Aims Irritable bowel syndrome (IBS) is a common disease characterized by intestinal dysmotility, the mechanism of which remains elusive. We aim to determine whether the high-affinity choline transporter 1 (CHT1), a determinant of cholinergic signaling capacity, modulates intestinal motility associated with stress-induced IBS. Methods A rat IBS model was established using chronic water avoidance stress (WAS). Colonic pathological alterations were evaluated histologically and intestinal motility was assessed by intestinal transit time and fecal water content (FWC). Visceral sensitivity was determined by visceromotor response to colorectal distension. RT-PCR, western blotting, and immunostaining were performed to identify colonic CHT1 expression. Contractility of colonic muscle strips was measured using isometric transducers. enzyme-linked immunosorbent assay was used to measure acetylcholine (ACh). We examined the effects of MKC-231, a choline uptake enhancer, on colonic motility. Results After 10 days of WAS, intestinal transit time was decreased and fecal water content increased. Visceromotor response magnitude in WAS rats in response to colorectal distension was significantly enhanced. Protein and mRNA CHT1 levels in the colon were markedly elevated after WAS. The density of CHT1-positive intramuscular interstitial cells of Cajal and myenteric plexus neurons in WAS rats was higher than in controls. Ammonium pyrrolidine dithiocarbamate partly reversed CHT1 upregulation and alleviated colonic hypermotility in WAS rats. Pharmacological enhancement of CHT1 activity by MKC-231 enhanced colonic motility in control rats via upregulation of CHT1 and elevation of ACh production. Conclusion Upregulation of CHT1 in intramuscular interstitial cells of Cajal and myenteric plexus neurons is implicated in chronic stress-induced colonic hypermotility by modulation of ACh synthesis via nuclear factor-kappa B signaling.

• Archives of Pharmacal Research
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• v.19 no.3
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• pp.201-206
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• 1996

Nitric oxide (NO) is thought to be a second messenger involved in secretion. Upon stimulating pancreatic acinar cells with cholecystokinin-pancreozymin (CCK-PZ), NO formation has been shown to be associated with increased levels of cGMP (Seo et al., 1995). To elucidate the signaling pathway of VIP-induced enzyme secretion, we investigated the NO and cGMP synthesis steps as potential steps where two signal pathways triggered by CCK-PZ and VIP interact. The results obtained in this work provide evidence that increase in pancreatic enzyme secretion by treatment with VIP has no relationship with NOS activity and cGMP level. This conclusion was derived from the following findings that VIP treatment of rat pancreatic tissue increased amylase release as well as protein output in a dose- and time-dependent manner, whereas NOS activity and cGMP synthesis were not affected by VIP treatment as monitored by NOS activity assay and determining cGMP level, which was further confirmed by a NOS-inhibitor study. Consequently, CCK-PZ or VIP increases enzyme secretion in rat pancreatic tissue, but the two hormones are different in their mode of action. Together the results suggest that signaling pathway of VIP-induced enzyme secretion might either bypass the NO and cGMP synthesis steps or lie on a distinct pathway from CCK-PZ-induced pathway.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.343.1-343.1
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• 2002

Nonsteroidal antiinflammatory drugs(NSAIDs) are widely used to treat pain. fever and inflammatory condition. But chronic-disease patients suffer from gastro-intestinal disturbances such as discomfort. nausea. peptic ulcer and severe bleeding because NSAIDs inhibit not only COX-2 associated with anti-inflammatory activity but also COX-1 associated with adverse gastro-intestinal effects. On the basis of this fact. specific COX-2 inhibitors such as celecoxib and rofecoxib are introduced in the drug market. (omitted)