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

Protein tyrosine phosphatase-22 (PTPN22) gene encodes lymphoid-specific tyrosine phosphatase (Lyp), an inhibitor of T cell activation. A polymorphism of the PTPN22 gene has been found to be associated with chronic urticaria (CU). We investigated the associations between PTPN22 gene polymorphisms and CU characteristics, including serum specific IgE antibodies response to toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A (SEA). CU patients (n=409) and normal healthy controls (n=388) were enrolled in the present study. Serum specific IgE to TSST-1 and SEA were measured by ImmunoCAP(R). Five PTPN22 single nucleotide polymorphisms, -1123G>C, 1858C>T, 13145A>G, 14943C>T, and 20628A>G, were genotyped. There were no significant differences in genotype or haplotype frequencies of these polymorphisms between the 2 groups. CU patients carrying the GG genotype at 20628A>G (P=0.035) or haplotype 3 [GGG] (P=0.047) had a significantly higher prevalence of serum specific IgE to TSST-1 compared to non-carriers. Similarly, CT/TT genotype at 14943C>T had a significantly higher prevalence of serum specific IgE to SEA (P=0.045). The findings suggest that the PTPN22 gene polymorphisms at 20628A>G and 14943C>T may enhance serum specific IgE responses to TSST-1 and SEA, which may contribute to CU pathogenesis.
Antibodies ; Enterotoxins ; Genotype ; Haplotypes ; Humans ; Immunoglobulin E* ; Polymorphism, Single Nucleotide ; Prevalence ; Shock, Septic ; Superantigens* ; Tyrosine ; Urticaria*

No abstract available.
Bacteroides fragilis* ; Bacteroides* ; Enterotoxins* ; Epithelial Cells* ; Gene Expression* ; Humans* ; Intestinal Mucosa*

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