• 제목/요약/키워드: intestinal inflammation

검색결과 192건 처리시간 0.023초

Intestinal Helminthic Infections Diagnosed by Colonoscopy in a Regional Hospital during 2001-2008

  • Do, Kyong-Rock;Cho, Young-Seok;Kim, Hyung-Keun;Hwang, Byung-Hee;Shin, Eun-Jung;Jeong, Hae-Bin;Kim, Sung-Soo;Chae, Hiun-Suk;Choi, Myung-Gyu
    • Parasites, Hosts and Diseases
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    • 제48권1호
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    • pp.75-78
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    • 2010
  • The present study investigated characteristics of 24 parasite infection cases detected during colonoscopy in a regional hospital from January 2001 to December 2008. Sixteen patients were confirmed with Trichuris trichiura infection, 6 patients were with Ascaris lumbricoides infection, 1 patient with Enterobius vermicularis infection, and 1 patient with Anisakis infection. Among them, 7 patients (43.8%) were asymptomatic. Colonoscopy findings were normal in 18 patients (75.0%). Among the patients with T. trichiura infection, colonoscopy showed several erosions in 2 patients (8.3%) and non-specific inflammation of the affected segment of the colon in 3 patients (12.5%). In 1 patient with anisakiasis, colonoscopy revealed a markedly swollen colonic wall. Stool examinations were performed before treatment in 7 patients (29.2%) and were all negative for parasite eggs or worms. These results suggest that colonoscopy is a useful diagnostic approach for parasitic infections even for asymptomatic patients and for patients with negative stool examinations.

항염증조절을 통한 자금정의 DSS 유도 궤양성 대장염 완화 효과 (Mitigating Effect of Jageum-jung on Dextran Sulfate Sodium-induced Ulcerative Colitis through Anti-inflammatory Regulation)

  • 최준용;안상현;사은호;사복석;김기봉
    • 대한한방내과학회지
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    • 제38권6호
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    • pp.944-954
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    • 2017
  • Objectives: This study investigated the anti-inflammatory effects of Jageum-jung extract on Dextran sulfate sodium (DSS-induced) ulcerative colitis in mice. Methods: Ulcerative colitis was induced by DSS in Balb/C male mice. Ten mice were assigned to each of four groups: Ctrl (control), UE (ulcerative colitis-induced), PT (treated with pentasaccharide after induction of ulcerative colitis), and JT (treated with Jageum-jung extract after induction of ulcerative colitis). The effects of Jageum-jung extract were measured by restoration of the length of the intestine, degree of mucosal damage as seen with histochemistry, and changes of p-IkB, iNOS, COX-2, and caspase-3 determined by immunohistochemistry. Results: The recovered intestinal length of the JT group was longer than that of the UE group. In the colon mucosa of JT group, hemorrhagic lesions were reduced, and the mucus barrier was recovered. This group also showed inhibited production of inflammatory enzymes (iNOS, COX-2) through regulation of proinflammatory enzyme (NF-kB, p65) activity in the colon. In addition, caspase 3 activation induced apoptosis. By GC/MS analysis, azetidine was identified. Conclusions: This study confirmed the anti-inflammatory effects of jageum-jung extract, and suggests the possibility of using Jageum-jung extract to treat ulcerative colitis. Further experiments and research on the mechanism of Jageum-jung effects are needed.

The effects of paeoniflorin injection on soluble triggering receptor expressed on myeloid-1 (sTREM-1) levels in severe septic rats

  • Liu, Xiao-Rong;Xu, Jie;Wang, Yi-Min;Ji, Ming-Suo;Liu, Fu-Shan
    • The Korean Journal of Physiology and Pharmacology
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    • 제20권6호
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    • pp.565-571
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    • 2016
  • Paeoniflorin (PAE) is the most abundant compound in Xuebijing injection widely used to treat sepsis. We aimed to investigate effect of PAE on expression of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) in a rat model of sepsis. Wistar rats were divided into Normal, Model, and PAE groups (n=20 each). Endotoxin was administrated at 5 mg/ml/kg in Model and PAE rats to establish rat sepsis model. 1 h after endotoxin administration, PAE was administrated at 4 ml/kg in PAE group once per day for 3 days. Routine blood tests and biochemical indexes were assessed, including aspartate aminotransferase (AST) and creatine kinase-MB (CK-MB). The plasma sTREM-1 level was measured using quantitative ELISA. At the end of experiment, the small intestine, liver, kidney and lung were subjected to pathological examinations. A rat model of sepsis-induced multiple organ dysfunction syndrome (MODS) was established successfully with endotoxin administration (5 mg/ml/kg), evidenced by histo-pathological examinations, routine blood tests and biochemical indexes: platelet count decreased and white blood cell count increased (p<0.05), CK-MB and AST increased (p<0.05). PAE treatment significantly reduced the plasma levels of AST, CK-MB, and sTREM-1, compared to Model group (p<0.05). Meanwhile, sepsis-induced damages in the liver, lung, stomach and intestinal mucosa were also markedly ameliorated by PAE treatment. PAE demonstrated a significantly protective effect in a rat model of sepsis by decreasing plasma sTREM-1 level, reducing inflammation, preventing MODS and protecting organ functions.

The Role of Gastrokine 1 in Gastric Cancer

  • Yoon, Jung Hwan;Choi, Won Suk;Kim, Olga;Park, Won Sang
    • Journal of Gastric Cancer
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    • 제14권3호
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    • pp.147-155
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    • 2014
  • Homeostatic imbalance between cell proliferation and death in gastric mucosal epithelia may lead to gastritis and gastric cancer. Despite abundant gastrokine 1 (GKN1) expression in the normal stomach, the loss of GKN1 expression is frequently detected in gastric mucosa infected with Helicobacter pylori, as well as in intestinal metaplasia and gastric cancer tissues, suggesting that GKN1 plays an important role in gastric mucosal defense, and the gene functions as a gastric tumor suppressor. In the stomach, GKN1 is involved in gastric mucosal inflammation by regulating cytokine production, the nuclear factor-${\kappa}B$ signaling pathway, and cyclooxygenase-2 expression. GKN1 also inhibits the carcinogenic potential of H. pylori protein CagA by binding to it, and up-regulates antioxidant enzymes. In addition, GKN1 reduces cell viability, proliferation, and colony formation by inhibiting cell cycle progression and epigenetic modification by down-regulating the expression levels of DNMT1 and EZH2, and DNMT1 activity, and inducing apoptosis through the death receptor-dependent pathway. Furthermore, GKN1 also inhibits gastric cancer cell invasion and metastasis via coordinated regulation of epithelial mesenchymal transition-related protein expression, reactive oxygen species production, and PI3K/Akt signaling pathway activation. Although the modes of action of GKN1 have not been clearly described, recent limited evidence suggests that GKN1 acts as a gastricspecific tumor suppressor. This review aims to discuss, comment, and summarize the recent progress in the understanding of the role of GKN1 in gastric cancer development and progression.

A Case of Human Pulmonary Dirofilariasis in a 48-Year-Old Korean Man

  • Kang, Hyo Jae;Park, Young Sik;Lee, Chang-Hoon;Lee, Sang-Min;Yim, Jae-Joon;Yoo, Chul-Gyu;Kim, Young Whan;Han, Sung Koo;Chai, Jong-Yil;Lee, Jinwoo
    • Parasites, Hosts and Diseases
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    • 제51권5호
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    • pp.569-572
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    • 2013
  • Dirofilariasis is a rare disease in humans. We report here a case of a 48-year-old male who was diagnosed with pulmonary dirofilariasis in Korea. On chest radiographs, a coin lesion of 1 cm in diameter was shown. Although it looked like a benign inflammatory nodule, malignancy could not be excluded. So, the nodule was resected by video-assisted thoracic surgery. Pathologically, chronic granulomatous inflammation composed of coagulation necrosis with rim of fibrous tissues and granulations was seen. In the center of the necrotic nodules, a degenerating parasitic organism was found. The parasite had prominent internal cuticular ridges and thick cuticle, a well-developed muscle layer, an intestinal tube, and uterine tubules. The parasite was diagnosed as an immature female worm of Dirofilaria immitis. This is the second reported case of human pulmonary dirofilariasis in Korea.

Prebiotics in the Infant Microbiome: The Past, Present, and Future

  • Miqdady, Mohamad;Mistarihi, Jihad Al;Azaz, Amer;Rawat, David
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • 제23권1호
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    • pp.1-14
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    • 2020
  • The latest definition of a prebiotic is "a substrate that is selectively utilized by host microorganisms conferring a health benefit"; it now includes non-food elements and is applicable to extra-intestinal tissues. Prebiotics are recognized as a promising tool in the promotion of general health and in the prevention and treatment of numerous juvenile diseases. Prebiotics are considered an immunoactive agent, with the potential for long-lasting effects extending past active administration of the prebiotic. Because of its extremely low risk of serious adverse effects, ease of administration, and strong potential for influencing the composition and function of the microbiota in the gut and beyond, the beneficial clinical applications of prebiotics are expanding. Prebiotics are the third largest component of human breast milk. Preparations including galactooligosaccharides (GOS), fructooligosaccharides (FOS), 2'-fucosyllactose, lacto-N-neo-tetraose are examples of commonly used and studied products for supplementation in baby formula. In particular, the GOS/FOS combination is the most studied. Maintaining a healthy microbiome is essential to promote homeostasis of the gut and other organs. With more than 1,000 different microbial species in the gut, it is likely more feasible to modify the gut microbiota through the use of certain prebiotic mixtures rather than supplementing with a particular probiotic strain. In this review, we discuss the latest clinical evidence regarding prebiotics and its role in gut immunity, allergy, infections, inflammation, and functional gastrointestinal disorders.

Helicobacter pylori Infection and Dietary Factors Act Synergistically to Promote Gastric Cancer

  • Raei, Negin;Behrouz, Bahador;Zahri, Saber;Latifi-Navid, Saeid
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권3호
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    • pp.917-921
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    • 2016
  • However, the incidence of gastric cancer (GC) has been decreased in past decades; GC is the second cause of cancer related death in the world. Evidence has illustrated that several factors including Helicobacter pylori (H. pylori) infection, host genetics, and environmental factors (smoking and particularly diet) may play a crucial role in gastric carcinogenesis. It has been demonstrated that high consumption of fresh fruits, vegetables, high level of selenium and zinc in drinking water, sufficient iron, and cholesterol protect against GC, while; smoked, pickled, and preserved foods in salt, and nitrites increase the risk of GC. Epidemiological studies have also proved that H. pylori infection and a high salt diet could independently induce atrophic gastritis and intestinal metaplasia. Recently, studies have been demonstrated that dietary factors directly influence H. pylori virulence. The use of appropriate diet could reduce levels of H. pylori colonization or virulence and prevent or delay development of peptic ulcers or gastric carcinoma. This is attractive from a number of perspectives including those of cost, treatment tolerability, and cultural acceptability. This review will describe new insights into the pathogenesis of H. pylori in relation to environmental factors, especially dietary, not only to find the developed means for preventing and treating GC, but also for understanding the role of chronic inflammation in the development of other malignancies.

Platelet Derived Growth Factor-B and Human Epidermal Growth Factor Receptor-2 Polymorphisms in Gall Bladder Cancer

  • Mishra, Kumudesh;Behari, Anu;Kapoor, Vinay Kumar;Khan, M. Salman;Prakash, Swayam;Agrawal, Suraksha
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권14호
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    • pp.5647-5654
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    • 2015
  • Gall bladder cancer (GBC) is a gastro-intestinal cancer with high prevalence among north Indian women. Platelet derived growth factor-B (PDGFB) and human epidermal growth factor receptor-2 (HER2) may play roles in the etiology of GBC through the inflammation-hyperplasia-dysplasia-carcinoma pathway. To study the association of PDGFB and HER2 polymorphisms with risk of GBC, 200 cases and 300 controls were considered. PDGFB +286A>G and +1135A>C polymorphisms were investigated with an amplification refractory mutation system and the HER2 $Ile^{655}Val$ polymorphism by restriction fragment length polymorphism. Significant risk associations for PDGFB +286 GG (OR=5.25) and PDGFB +1135 CC (OR=3.19) genotypes were observed for GBC. Gender wise stratification revealed susceptibility for recessive models of PDGFB +1135A>C (OR=3.00) and HER2 $Ile^{655}Val$ (OR=2.52) polymorphisms among female GBC cases. GBC cases with gall stones were predisposed to homozygous +286 GG and +1135 CC genotypes. Significant risk associations were found for ACIle (OR=1.48), GAVal (OR=1.70), GAIle (OR=2.00) haplotypes with GBC cases and GCIle haplotype with female GBC cases (OR=10.37, P=<0.0001). Pair-wise linkage disequilibrium revealed negative associations among variant alleles. On multi-dimensional reduction analysis, a three factor model revealed significant gene-gene interaction for PDGFB +286A>G, PDGFB +1135A>C and HER2 Ile165Val SNPs with GBC. Protein-protein interaction showed significant association of PDGFB and HER2 with the epidermal growth factor receptor signaling pathway.

Evaluation of Enterotoxigenic Bacteroides fragilis from Colonic Washings from Patients Undergoing Colonoscopy

  • Van, Ni;Ahlberg, Ned;Jung, Byung Chul;Lee, Min Ho;Ahn, Seung Ju;Lee, In-Soo;Kim, Yoon Suk;Rhee, Ki-Jong
    • 대한의생명과학회지
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    • 제18권4호
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    • pp.362-368
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    • 2012
  • Enterotoxigenic Bacteroides fragilis (ETBF) is an intestinal commensal bacterium implicated as a risk factor for colon cancer. The key virulence factor is a secreted toxin called B. fragilis toxin (BFT). In this study we used an in vitro bioassay to examine the prevalence of ETBF in colonic washings from patients with colorectal polyps and normal control patients. We found that 9.3% of polyp patients and 10.9% of non-polyp patients harbored ETBF, respectively. A total of nine ETBF clinical isolates were isolated and confirmed to be positive for the BFT gene by PCR analysis and the ability to induce IL-8 secretion in the colonic epithelial cell line HT29/c1. Two of the ETBF clinical strains were characterized further in vitro and in vivo. We found that the two ETBF clinical isolates induced E-cadherin cleavage in HT29/c1 cells and promoted colonic inflammation in C57BL/6 mice. Our results indicate that the prevalence of ETBF in polyp patients were similar in non-polyp patients suggesting that ETBF carriage does not positively correlate to polyp incidence.

Oral administration of fermented wild ginseng ameliorates DSS-induced acute colitis by inhibiting NF-κB signaling and protects intestinal epithelial barrier

  • Seong, Myeong A;Woo, Jong Kyu;Kang, Ju-Hee;Jang, Yeong Su;Choi, Seungho;Jang, Young Saeng;Lee, Taek Hwan;Jung, Kyung Hoon;Kang, Dong Kyu;Hurh, Byung Seok;Kim, Dae Eung;Kim, Sun Yeou;Oh, Seung Hyun
    • BMB Reports
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    • 제48권7호
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    • pp.419-425
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    • 2015
  • Ginseng has been widely used for therapeutic and preventive purposes for thousands of years. However, orally administered ginseng has very low bioavailability and absorption in the intestine. Therefore, fermented ginseng was developed to enhance the beneficial effects of ginseng in the intestine. In this study, we investigated the molecular mechanisms underlying the anti-inflammatory activity of fermented wild ginseng (FWG). We found that FWG significantly alleviated the severity of colitis in a dextran sodium sulfate (DSS)-induced colitis mouse model, and decreased expression level of pro-inflammatory cytokines in colonic tissue. Moreover, we observed that FWG suppressed the infiltration of macrophages in DSS-induced colitis. FWG also attenuated the transcriptional activity of nuclear factor-κB (NF-κB) by reducing the translocation of NF-κB into the nucleus. Our data indicate that FWG contains anti-inflammatory activity via NF-κB inactivation and could be useful for treating colitis. [BMB Reports 2015; 48(7): 419-425]