• Journal of Microbiology
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• v.43 no.2
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• pp.133-143
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• 2005

Shigellosis is a global human health problem. Four species of Shigella i.e. S. dysenteriae, S. flexneri, S. boydii and S. sonnei are able to cause the disease. These species are subdivided into serotypes on the basis of O-specific polysaccharide of the LPS. Shigella dysenteriae type 1 produces severe disease and may be associated with life-threatening complications. The symptoms of shigellosis include diarrhoea and/or dysentery with frequent mucoid bloody stools, abdominal cramps and tenesmus. Shigella spp. cause dysentery by invading the colonic mucosa. Shigella bacteria multiply within colonic epithelial cells, cause cell death and spread laterally to infect and kill adjacent epithelial cells, causing mucosal ulceration, inflammation and bleeding. Transmission usually occurs via contaminated food and water or through person-to-person contact. Laboratory diagnosis is made by culturing the stool samples using selective/differential agar media. Shigella spp. are highly fragile organism and considerable care must be exercised in collecting faecal specimens, transporting them to the laboratories and in using appropriate media for isolation. Antimicrobial agents are the mainstay of therapy of all cases of shigellosis. Due to the global emergence of drug resistance, the choice of antimicrobial agents for treating shigellosis is limited. Although single dose of norfloxacin and ciprofloxacin has been shown to be effective, they are currently less effective against S. dysenteriae type 1 infection. Newer quinolones, cephalosporin derivatives, and azithromycin are the drug of choice. However, fluoroquinolone-resistant S. dysenteriae type 1 infection have been reported. Currently, no vaccines against Shigella infection exist. Both live and subunit parenteral vaccine candidates are under development. Because immunity to Shigella is serotype-specific, the priority is to develop vaccine against S. dysenteriae type 1 and S. flexneri type 2a. Shigella species are important pathogens responsible for diarrhoeal diseases and dysentery occurring all over the world. The morbidity and mortality due to shigellosis are especially high among children in developing countries. A recent review of literature (KotIoff et al.,1999) concluded that, of the estimated 165 million cases of Shigella diarrhoea that occur annually, $99\%$ occur in developing countries, and in developing countries $69\%$ of episodes occur in children under five years of age. Moreover, of the ca.1.1 million deaths attributed to Shigella infections in developing countries, $60\%$ of deaths occur in the under-five age group. Travellers from developed to developing regions and soldiers serving under field conditions are also at an increased risk to develop shigellosis.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.12 no.2
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• pp.177-182
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• 2009

Purpose: Colitis is a condition associated with a spectrum of altered morphologic changes and cellular adhesion. E-cadherin plays a key role in the establishment and maintenance of epithelial tissue structure and cell-cell adhesion. The purpose of this study is to evaluate E-cadherin expression in colonic epithelium of various colitis in children. Methods: The expressions of E-cadherin were examined in 39 cases of colonic mucosal biopsy specimen using immunohistochemical staining. When more than 50 percent of cells exhibited uniformly the same intensity and pattern of immunostaining as the adjacent normal mucosa, the antigen expression was considered normal. Abnormal expression was defined when less than 50 percent of cells stained, when cells showed a heterogeneously weak or altered distribution, or when complete absence of staining was observed. Results: Fifteen cases with non-specific colitis (38.5%), 7 cases of with Crohn's disease (17.9%), 5 cases of infectious colitis and milk protein sensitive proctocolitis (12.8%), 3 cases of ulcerative colitis (7.7%), 2 cases of Henoch-Schonlein purpura colitis (5.1%), one case of Behcet's disease and ischemic colitis (2.6%) were included in this study. E-cadherin expression was decreased in all kinds of colitis. Reduced expression of E-cadherin was observed in 77 percent of cases. E-cadherin was weaker or no expression in reparative epithelium and "ulcer associated cell lineage". Conclusion: Altered expression of E-cadherin occurs during mucosal inflammation in any kinds of colitis. These changes may be involved in promoting cell migration during epithelial restitution of the gastrointestinal mucosa.

• Journal of Environmental Science International
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• v.29 no.3
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• pp.241-247
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• 2020

Ulmus davidiana Nakai (UDN) has been traditionally used as a herbal medicine in Korea. In the present study, we investigated the anti-ecotoxic potential of a 116 kDa glycoprotein isolated from UDN (UDN glycoprot ein) in regulating fecal malodor and feed efficiency in mice. We found that UDN glycoprotein (200 μg/ml) has an inhibitory effect on the cell death induced by an ecotoxicological endocrine disrupting chemical, bisphenol A, in colon epithelial HT-29 cells. UDN glycoprotein did not show significant differences regarding the weight of ecotoxicity-related organs (liver, heart, kidneys, and spleen) and the levels of serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, and lactate dehydrogenase in mice for 2 weeks, compared to the control. Additionally, UDN glycoprotein reduced the levels of hydrogen sulfide and ammonia as markers of fecal malodor in mice. Interestingly, UDN glycoprotein can improve the mouse feed efficiency. In conclusion, our data indicate that anti-ecotoxicological UDN glycoprotein has the ability to increase the feed efficiency and reduce the fecal malodor by maintaining the viability of colonic epithelial cells in mice.

• Biomedical Science Letters
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• v.18 no.4
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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.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.3
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• pp.1023-1035
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• 2016

The purpose of this study was to investigate the role of colon cancer stem cells (CSCs) during chemically-induced rat multi-step colon carcinogenesis with or without the treatment with a specific cyclooxygenase-2 inhibitor drug (celecoxib). Two experiments were performed, the first, a short term 12 week colon carcinogenesis bioassay in which only surrogate markers for colon cancer, aberrant crypt foci (ACF) lesions, were formed. The other experiment was a medium term colon cancer rat assay in which tumors had developed after 32 weeks. Treatment with celecoxib lowered the numbers of ACF, as well as the tumor volumes and multiplicities after 32 weeks. Immunohistochemical proliferating cell nuclear antigen (PCNA) labeling indexes LI (%) were downregulated after treatment by celecoxib. Also different cell surface antigens known to associate with CSCs such as the epithelial cell adhesion molecule (EpCAM), CD44 and CD133 were compared between the two experiments and showed differential expression patterns depending on the stage of carcinogenesis and treatment with celecoxib. Flow cytometric analysis demonstrated that the numbers of CD133 cells were increased in the colonic epithelium after 12 weeks while those of CD44 but not CD133 cells were increased after 32 weeks. Moreover, aldehyde dehydrogenase-1 activity levels in the colonic epithelium (a known CSC marker) detected by ELISA assay were found down-regulated after 12 weeks, but were up-regulated after 32 weeks. The data have also shown that the protective effect of celecoxib on these specific markers and populations of CSCs and on other molecular processes such as apoptosis targeted by this drug may vary depending on the genetic and phenotypic stages of carcinogenesis. Therefore, uncovering these distinction roles of CSCs during different phases of carcinogenesis and during specific treatment could be useful for targeted therapy.

• Journal of Veterinary Clinics
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• v.15 no.1
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• pp.203-208
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• 1998

A two-year-old male Chinese Shar poi dog was admitted to the hospital because of chronic diarrhea. Abnormalities detected on physical examination were thickened intestinal loops and thin or cachexic body condition.4 complete blood count revealed a mild neutrophilia. The blood chemistry panel indicated no significant abnormalities. On proctoscopic examinations colonic mucosa was reddened and edematous. Numerous Iymphocytes, plasma cells and epithelial cells were observed in the cytologic examination of the rectal scraping.4 treatment was initiated with sulfasalazinei metronidazole and prednisolone and dietary management with rice and cottage cheese was performed simultaneously. Although antibiotic therapy and dietary management were donee the dog's condition deteriorated and died suddenly. Lymphocytic-plasmacytic enterocolitis was diagnosed by postmortem pathologic examination.

• Journal of Microbiology and Biotechnology
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• v.26 no.8
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• pp.1446-1451
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• 2016

Clostridium difficile toxin A causes acute gut inflammation in animals and humans. It is known to downregulate the tight junctions between colonic epithelial cells, allowing luminal contents to access body tissues and trigger acute immune responses. However, it is not yet known whether this loss of the barrier function is a critical factor in the progression of toxin A-induced pseudomembranous colitis. We previously showed that NADH:quinone oxidoreductase 1 (NQO1) KO (knockout) mice spontaneously display weak gut inflammation and a marked loss of colonic epithelial tight junctions. Moreover, NQO1 KO mice exhibited highly increased inflammatory responses compared with NQO1 WT (wild-type) control mice when subjected to DSS-induced experimental colitis. Here, we tested whether toxin A could also trigger more severe inflammatory responses in NQO1 KO mice compared with NQO1 WT mice. Indeed, our results show that C. difficile toxin A-mediated enteritis is significantly enhanced in NQO1 KO mice compared with NQO1 WT mice. The levels of fluid secretion, villus disruption, and epithelial cell apoptosis were also higher in toxin A-treated NQO1 KO mice compared with WT mice. The previous and present results collectively show that NQO1 is involved in the formation of tight junctions in the small intestine, and that defects in NQO1 enhance C. difficile toxin A-induced acute inflammatory responses, presumably via the loss of epithelial cell tight junctions.

• Korean Journal of Veterinary Research
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• v.33 no.3
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• pp.429-442
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• 1993

The cytotoxic effects of S hyodysenteriae strain B 204 on the mucosal surface were studied in surgically prepared ligated colonic loops in two male convenitonal mixed-breed pigs. In each one of four loops was inoculated with either sterile trypticase soy broth(TSB) of Serpulina, filtrate of Serpulina TSB culture. washed Serpulina cells or whole culture of Serpulina. Mucosal tissues were examined by transmission and scanning electron microscopy 24 and 48 hours after inoculation(p.i.). The filtrate did not induce any significant effect on the mucosal surface. The washed cells produced early lesions similar to those caused by the whole culture. These observations suggest that cytotoxins of the culture do not play a significant role in invasion of the epithelium in this experimental infection. The possible role of toxins associated with the organism at the site of interaction with the epithelial cells was not elucidated.

• YAKHAK HOEJI
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• v.54 no.2
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• pp.91-96
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• 2010

Berberine, an isoquinoline alkaloid, has a wide range of pharmacological effects, including anti-inflammation. It has been reported that berberine inhibits experimental colitis through inhibition of IL-8, and that inhibitory effect of berberine on inflammatory cytokine expression is mediated through peroxisome proliferator activated receptor (PPAR)-$\gamma$. In this study, we examined the effects and action mechanism of berberine on the tumor necrosis factor (TNF)-$\alpha$-induced monocyte adhesion to HT29 human colonic epithelial cells, which is commonly used as an in vitro model of inflammatory bowel disease (IBD). Berberine significantly inhibited the TNF-$\alpha$-induced monocyte adhesion to HT29, which is similar to the effect of PDTC, a nuclear factor (NF)-$\kappa$B inhibitor. However, ciglitazone and GW, the ligands of PPAR-$\gamma$, did not suppress the TNF-$\alpha$-induced monocyte adhesion to HT29 cells. In addition, TNF-$\alpha$-induced chemokine expression and NF-$\kappa$B transcriptional activity were significantly inhibited by berberine in a concentration-dependent manner. The results suggest that inhibitory effect of berberine on colitis is mediated through suppression of NF-$\kappa$B and NF-$\kappa$B-dependent chemokine expression.

• Clinical and Experimental Pediatrics
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• v.50 no.12
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• pp.1257-1260
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• 2007

E. histolytica has a simple life cycle with two stages: an infective cyst and an invasive trophozoite. It lives on humans as its host. Its infection occurs through the ingestion of the cyst form, and the disease begins when the trophozoite, converted at the small intestine, adheres to colonic epithelial cells with a latent period of two days to four months. In some instances, amoebic abscess formations can occur at the liver, lung, brain, or spleen via the lymphoid system. Rare cases of amoebiasis in neonates have been reported, much less any intrauterine infections in the world that may have occurred during the gestation period. We've recently experienced a case of neonatal amoebiasis that entailed after-birth vomiting and bloody stool. The infant seemed pre-infected with E. histolytica before birth.