Melatonin attenuates thioacetamide-induced liver fibrosis in male rats through modulation of interleukin-6, interleukin-4, apoptosis and urokinase plasminogen activator receptor-associated protein/Endo180.

Liver fibrosis is a chronic progressive disease, its resolution still unclear, and the current study explored the role of melatonin in modulation of interleukin-6 (IL-6), interleukin-4 (IL-4), transforming growth factor beta1 (TGF-ß1) and urokinase plasminogen activator receptor-associated protein/Endo180 (uPARAP/Endo180) pathway in thioacetamide (TAA)-induced hepatotoxicity. Thirty two adult Sprague-Dawley rats were divided into four groups: vehicle control group, TAA-induced liver fibrosis group that was left untreated, melatonin administration before and along with TAA and melatonin along with TAA group. TTA-induced massive liver necrosis, fibrosis around portal tract and increases serum levels of liver enzymes and total bilirubin when compared with control vehicle group. While both melatonin pretreatment and treatment retained liver parenchyma and liver enzymes quite similar to control group and reduced TAA-induced liver injury. Notably, melatonin pretreatment and treatment increased collagen degradation in TAA liver injury by19, 31.7-fold respectively evidence by collagen percentage area. Melatonin also decreased the amount of thiobarbituric acid reactive compounds and retained the reduced glutathione and superoxide dismutase to basal level quite similar to control group. Additionally, melatonin significantly (P value ≤0.05) decreased the levels of TGF-ß1, epidermal growth factor (EGF), hydroxyproline, tissues IL-6, caspase-3, and receptor interacting serine/threonine kinase1 (RIPK1), fibrillin-1, and - smooth muscle actin in the liver tissues while significantly (P value ≤0.05) increasing the levels of IL-4 and uPARAP/Endo180. Due to its anti-inflammatory, anti-apoptotic, and antioxidant capabilities as well as its ability to decrease hepatic stellate cell activation and fibrogenesis, these data imply that melatonin has a powerful anti-fibrotic effect.

Enteropathogenic Escherichia coli (EPEC): Does it have a role in colorectal tumourigenesis? A Prospective Cohort Study.

BACKGROUND: Despite the characterization of many aetiologic genetic changes. The specific causative factors in the development of sporadic colorectal cancer remain unclear. This study was performed to detect the possible role of Enteropathogenic Escherichia coli (EPEC) in developing colorectal carcinoma. PATIENTS AND METHOD: Fresh biopsy specimens have been obtained from the colonic mucosa overlying the colorectal cancer as well as from the colon of the healthy controls. Culture, genotyping and virulence of EPEC were done using (nutrient broth culture, and PCR). Strains biochemically identified as Escherichia coli were selected from the surface of a MacConkey's plate and were serogrouped by slide agglutination tests. RESULTS: From January 2011 to June 2014, 213 colorectal cancer patients (Group 1) and 248 healthy controls (Group 2) were prospectively enrolled in this study. EPEC was positive in 108 (50.7%) in group 1 and 51 (20.6%) in group 2 (P = 0.0001). A significant difference between both groups was observed regarding serotyping, genotyping (eae gene) and virulence category (P = 0.0001). A significant difference between the 2 subgroups of colorectal cancer cases was observed regarding genotyping (eae, bfb genes) and virulence category. CONCLUSION: The incidence EPEC was higher significantly in patients with colorectal cancer. E. coli in patients with colorectal cancer significantly differed serotypically and genotypically from the E. coli in normal population. E. coli colonization of the colonic mucosa may be a cause colorectal cancer.

Multilocus genotypic characterization of Escherichia coli O157:H7 recovered from food sources.

Escherichia coli O157:H7 strains (n = 33) recovered from different food sources in Egypt were characterized using molecular assays to identify strain genotypes associated with various levels of pathogenic potential. Genotypic characterization included: lineage-specific polymorphism assay (LSPA-6), Shiga-toxin-encoding bacteriophage insertion site assay (SBI), clade 8 typing, Tir (A255 T) polymorphism, and variant analysis of Shiga toxin 2 gene (Stx 2a and Stx 2c), and anti-terminator Q genes (Q 933 and Q 21). Genotypes LI/II (76%), SBI 1 (60·6%), clade 8 (69·7%), Tir (255 T) (72·7%) and Stx 2c (45·5%) were found to be significantly more frequent compared to other genetic markers in the strains analysed. Multivariable analysis revealed a significant association between LPSA-6 and clade types as well as Tir (A255 T). To the best of our knowledge, this is the first study to report the characterization of these genetic markers in E. coli O157:H7 strains in the Middle East and Africa.

Biofilm mediates Enterococcus faecalis adhesion, invasion and survival into bovine mammary epithelial cells.

UNLABELLED: We proposed in this study that during intramammary infection, biofilm formation may facilitate adherence and colonization of Enterococcus faecalis to mammary gland epithelium. This was established by comparing six different Ent. faecalis isolates with different biofilm-forming profiles for their adhesive, invasive and survival capabilities to bovine mammary epithelial cell line (MAC-T). Our results showed increased ability of the biofilm-producer Ent. faecalis strains to adhere, invade and survive inside MAC-T cells rather than nonbiofilm-producer strains. We showed that growth of bacteria in bovine milk significantly augmented the adherence and invasion of all tested strains, and this feature was abolished again when strains were subcultured in brain heart infusion broth. Moreover, growth in bovine milk significantly increased biofilm formation by all tested strains. These results indicated that biofilm formation by Ent. faecalis, especially after expressing milk-dependent induction, may have special relevance in the pathogenesis of Ent. faecalis mastitis during intramammary infection by enhancing bovine mammary epithelial adhesion and colonization. SIGNIFICANCE AND IMPACT OF THE STUDY: Results obtained from current work highlighted the role of biofilm in the pathogenesis of Enterococcus faecalis mastitis. Those biofilm-forming strains might be substantial as useful antigens in diagnostic assays and as future vaccine candidates to control Ent. faecalis mastitis.

Shiga toxin-producing Escherichia coli from raw milk cheese in Egypt: prevalence, molecular characterization and survival to stress conditions.

Raw milk cheese is considered as a risk for foodborne Shiga toxin-producing E. coli (STEC) contamination. In this study, 124 raw milk cheese samples (64 Kareish and 60 Damietta cheese samples) were assayed for the presence of STEC using molecular detection of virulence markers such as Shiga toxins (stx1 and st×2) and intimin gene (eae) and by serotyping. By PCR, 14 E. coli strains showed the presence of the stx2 gene, either single or in association with the stx1, and were considered positive for STEC. The isolated non-O157 STEC in this study (from serotypes O22:H8, O26:H11, O86:H21, O103:H2, O113:H21 and O146:H21) were inoculated in 10% skim milk and were compared to O157:H7 reference strain for their survival under different stress conditions (pH levels between 4·5 and 6·5 and salt concentrations between 1 and 6%) and 8 days of storage at refrigeration temperature (4°C). Strikingly, our results showed that O26:H11 survived significantly better than O157:H7 under acidic pH and higher salt concentration.