Data Availability StatementAll data generated or analyzed during the present study

Data Availability StatementAll data generated or analyzed during the present study are included in this published article. by Shiga toxin. In conclusion, the findings of the present study demonstrated that colonization by strains can inhibit EHEC infection. O157:H7, germ-free mice, intestinal flora Introduction Enterohemorrhagic (EHEC) is one of the most common pathogenic intestinal bacteria worldwide. EHEC RICTOR is a food-borne zoonotic pathogen associated with outbreaks that pose a major public health concern worldwide. Once EHEC is ingested, it produces and releases Shiga toxin (Stx) (1). Stx is one of the most important pathogenic factors in EHEC infections (2). Stx binds to globotriaosylceramide (Gb3), which is a Stx receptor expressed in the intestinal epithelium and on the surface of endothelial cells (2). After Stx binds to buy STA-9090 Gb3, it inhibits protein synthesis and induces cell apoptosis (1). Gb3 is also expressed on vascular endothelial cells and nerve cells. Once Stx enters the bloodstream, it may lead to kidney and brain injury (3,4). Stx comprises Stx1 and Stx2(1). Stx1 has the same structure as the Shiga toxin produced by (1), whereas Stx2 has a different structure (5), and it has been reported that Stx2 is associated with the severity of buy STA-9090 EHEC infection (5). EHEC colonizes the colon and causes diarrhea, hemorrhagic colitis and hemolytic uremic syndrome (HUS) or encephalopathy in humans (6,7). EHEC has several serotypes (8), and buy STA-9090 EHEC O157:H7 is the strain with the highest rate of isolation (1). In 1982, EHEC O157:H7 was isolated and identified in America as a food-borne pathogen (1). It was the first identification of a food-borne pathogen causing worldwide colitis outbreaks (9). In 1996, a big outbreak of EHEC O157:H7 infection occurred, starting with a school lunch in Japan (10). Therefore, EHEC O157:H7 has been recognized as one of the most serious food-borne pathogens. In a previous study, it was reported that the susceptibility to EHEC infection varies among different individuals, with infants, children and the elderly being highly susceptible (11). In particular, patients younger than 5 years are at high risk for the buy STA-9090 development of severe symptoms, such as HUS (11). Cattle are major carriers of EHEC; however, EHEC colonization in adult ruminants is asymptomatic (1). While EHEC colonizes the colon of humans and forms pathological lesions, it may colonize the recto-anal junction of cattle without Stx-related manifestations (1). The differential susceptibility to Stx and selectivity in colonization sites are associated with host tolerance to EHEC. Cattle transmit EHEC to humans by shedding the pathogen in the feces. Fecal shedding leads to contamination of farm environments by EHEC (12). In a recent study, Wang investigated the role of the microbiome in EHEC shedding, and indicated that shedding is affected by the composition of the microbiome (12). In particular, it was demonstrated that Firmicutes, Bacteroidetes and Proteobacteria promote EHEC shedding. These phyla also represent the predominant microorganisms in the human and mouse gut microbiome (13). Therefore, it was suggested that these strains may play an important role in EHEC infection in humans and mice. Intestinal microbiota play an important role in protecting hosts from enteric infections. It has been reported that gastrointestinal microbiota act protectively against enteric infections (14-16). Furthermore, the susceptibility to EHEC infections is affected by the composition of the intestinal microbiome in mice (17). Several studies have investigated the association between specific bacterial strains and EHEC infection (18-23), focusing on probiotic strains. Probiotics are live organisms that, when ingested in adequate amounts, confer a health benefit on the host (24). By protecting the host from pathogen colonization (23) and modulating host immune response (25), probiotic bacteria can contribute to the defense.

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