No abstract available.
Aeromonas* ; Enterotoxins*

No abstract available.
Enterotoxigenic Escherichia coli* ; Enterotoxins*

No abstract available.
Enterotoxigenic Escherichia coli* ; Enterotoxins*

No abstract available.
Cholera* ; Enterotoxins* ; Korea* ; Vibrio cholerae* ; Vibrio*

No abstract available.
Bacteroides fragilis* ; Bacteroides* ; Enterotoxins* ; Epithelial Cells* ; Humans* ; Signal Transduction*

Claudin proteins are the most crucial components of tight junctions, and play an essential role in maintaining cell polarity, regulating cell permeability and the intercellular ion. In recent years, many studies have shown that abnormality of claudins expression is implicated in the tumor progression. The expression correlates with tumor prognosis and can serve as a biomarker of prognosis and potential therapeutic targets. This review summarizes the current knowledge regarding claudin dysregulation in cancer and highlights the progress in claudin-based treatments.
Claudins ; therapeutic use ; Enterotoxins ; Humans ; Neoplasms ; drug therapy ; Tight Junctions

BACKGROUND AND OBJECTIVE: Atopic dermatitis(AD) is a chronic inflammatory skin disease with a high incidence in early childhood. Staphylococcus aureus(SA) is found at high concentrations in over 90% of AD skin lesions compared with 5-37% of age-matched controls. SA isolates from AD subjects have a high prevalence(37-57%) of superantigen-producing strains. And staphylococcal enterotoxin B(SEB) has been shown to induce inflammatory reactions following application to intact skin of normal and atopic subjects. These findings suggest that SA toxin produced by SA may be linked with initiation or aggravation of AD, but the role of satphylococcal enterotoxin to the T cell in the pathogenesis of AD has not been determined clearly. This study was conducted to determine whether staphylococcal enterotoxin might have a role as a superantigen in the pathogenesis of AD. Materials and Method: We investigated the proliferative responses of peripheral blood mononuclear cell(PBMC) from 8 patients with AD and 10 age-matched normal controls. We also assessed T cell markers and T cell receptor(TCR) Vbeta chain expression by flow cytometry with and without SEB stimulation. RESULTS: PBMC from AD patients showed increased proliferation to SEB 100 pg/ml and 1000 pg/ml compared to controls. There were no differences of CD3(+), CD4(+), and CD8(+) cells after SEB stimulation between the two groups. And there were also no differences of TCR Vbeta2(+) and TCR Vbeta8(+) cells with and without SEB stimulation, but TCR Vbeta17(+) cells were increased after SEB stimulation not only in AD patients but also in controls compared to culture without SEB. The expressions of TCR Vbeta17 chain of CD3(+) and CD4(+) cells after SEB stimulation were increased in AD patients compared to controls. Furthermore, there was positive correlation between the enhanced PBMC proliferative responses to SEB and increased expressions of SEB reactive TCR Vbeta17(+)/CD4(+) cells in AD patients and controls. CONCLUSION: These findings suggest that SEB is important in the pathogenesis of atopic dermatitis and also provide evidence that the increased use of certain TCR Vbeta families is of functional significance.
Dermatitis, Atopic* ; Enterotoxins* ; Flow Cytometry ; Humans ; Incidence ; Skin ; Skin Diseases ; Staphylococcus

OBJECTIVES: It has been proposed that microbial persistence, superantigen (SA) production, and host T-cell response may be involved in the development of chronic rhinosinusitis. According to the SA hypothesis, a single intranasal application of SA such as staphylococcal enterotoxin B (SEB) may induce chronic eosinophilic rhinosinusitis. This study aimed to develop a rat model of rhinosinusitis induced by intranasally applied SEB. METHODS: Forty microliter of SEB (100 microgram/mL) or phosphate buffered saline was applied intranasally through each naris in 4 weekold Sprague-Dawley test rats (N=36) and controls (N=16), respectively. Following sacrifice at 1, 5, 14, and 28 days, the obtained nasal cavity and sinuses were prepared for histologic investigation. The histologic sections were examined in a blind manner for the ratio of the sinus spaces occupied by inflammatory cell clusters and the number of inflammatory cells in the lamina propria. RESULTS: Infiltration of neutrophils in the lamina propria and appearance of neutrophil clusters in the sinus spaces were observed in the SEB-applied rats. The ratio of the sinus spaces occupied by neutrophil clusters and the number of neutrophils infiltrated in the lamina propria increased significantly at day 1 as compared with the control rats. CONCLUSION: Intranasally applied SEB induces acute neutrophilic rhinosinusitis in rats. Eosinophilic inflammation was not demonstrated. The mere presence of SA in the nose does not necessarily induce SA-induced inflammation, as suggested by the SA hypothesis.
Animals ; Enterotoxins ; Eosinophils ; Inflammation ; Mucous Membrane ; Nasal Cavity ; Neutrophils ; Nose ; Rats ; Sinusitis ; T-Lymphocytes

OBJECTIVES: It has been proposed that microbial persistence, superantigen (SA) production, and host T-cell response may be involved in the development of chronic rhinosinusitis. According to the SA hypothesis, a single intranasal application of SA such as staphylococcal enterotoxin B (SEB) may induce chronic eosinophilic rhinosinusitis. This study aimed to develop a rat model of rhinosinusitis induced by intranasally applied SEB. METHODS: Forty microliter of SEB (100 microgram/mL) or phosphate buffered saline was applied intranasally through each naris in 4 weekold Sprague-Dawley test rats (N=36) and controls (N=16), respectively. Following sacrifice at 1, 5, 14, and 28 days, the obtained nasal cavity and sinuses were prepared for histologic investigation. The histologic sections were examined in a blind manner for the ratio of the sinus spaces occupied by inflammatory cell clusters and the number of inflammatory cells in the lamina propria. RESULTS: Infiltration of neutrophils in the lamina propria and appearance of neutrophil clusters in the sinus spaces were observed in the SEB-applied rats. The ratio of the sinus spaces occupied by neutrophil clusters and the number of neutrophils infiltrated in the lamina propria increased significantly at day 1 as compared with the control rats. CONCLUSION: Intranasally applied SEB induces acute neutrophilic rhinosinusitis in rats. Eosinophilic inflammation was not demonstrated. The mere presence of SA in the nose does not necessarily induce SA-induced inflammation, as suggested by the SA hypothesis.
Animals ; Enterotoxins ; Eosinophils ; Inflammation ; Mucous Membrane ; Nasal Cavity ; Neutrophils ; Nose ; Rats ; Sinusitis ; T-Lymphocytes

This study was aimed to investigate the effect of clostridium difficile toxin A (Tcd A) on proliferation of K562 cells and its mechanism. The proliferative activity of K562 cells exposed to Tcd A was tested by MTT assay; cell cycle distribution and mitochondrial membrane potential were analyzed by flow cytometry; the protein expression of cytochrome C and DNA fragmentation were observed by immunohistochemistry staining and agarose gel electrophoresis respectively. The results indicated that Tcd A inhibited proliferation of K562 cells in a time-and concentration-dependent manner. Cells were arrested at G(0)/G(1) phase. Peak of apoptosis appeared. The protein expression of cytochrome C increased as compared with control group (p < 0.05). Agarose gel electrophoresis of DNA from K562 treated with Tcd A revealed a "ladder" pattern. It is concluded that clostridium difficile toxin A can inhibit proliferation and induce apoptosis of K562 cells. The mechanism may be in relation to decrease of mitochondrial membrane potential and the release of cytochrome C from mitochondria matrix.
Apoptosis ; drug effects ; Bacterial Toxins ; pharmacology ; Cell Proliferation ; drug effects ; Enterotoxins ; pharmacology ; Humans ; K562 Cells