JRK carried out the primer design to differentiate C. jejuni from C. coli. OAO conceived and coordinated the study, designed and revised #GF120918 molecular weight randurls[1|1|,|CHEM1|]# the manuscript. All authors read and accepted the final version of the manuscript.”
“Background Diarrheal infections caused by bacterial enteric pathogens including Salmonella, are one of the major causes of

childhood morbidity and mortality in developing countries [1]. Salmonella enterica serovar Typhimurium (S. Typhimurium) is an intracellular Gram-negative bacterium characterized by its ability to survive and replicate within eukaryotic host cells, particularly epithelial cells and macrophages. In humans, while Salmonella enterica serovar Typhi typically causes severe or sometimes lethal systemic illness called “”Typhoid BIBF1120 Fever”", Salmonella Typhimurium is associated with self limiting gastroenteritis and requires treatment only in immunocompromised patients. S. Typhimurium develops in mice an infection with the same pathogenesis and clinical manifestations than S. Typhi in humans thus, this mouse model is useful for the study of this disease [2]. The intestine harbours trillions of commensal bacteria that participate in digestive functions and help to protect the host from the aggression of several enteropathogens [3]. The beneficial effects of the microbiota on the host immune system have allowed the proposal to use some non pathogenic bacteria, such as probiotics in improving

animal health and protection against infectious agents [4]. Probiotics have been shown to influence both innate and adaptive immunity through direct contact with epithelial and immune cells, or by their ability to modify the composition and activity of the gut microbiota. They exert their protective effects by multiple immune and non immune mechanisms [5], i.e., exerting direct antimicrobial activity against pathogens [6], increasing phagocytosis

[7], modifying cytokine production by different cell populations [8–10] or enhancing IgA production [11]. One of the principal mechanisms of protection against gastroenteric infections by probiotics is via modulation of pro-inflammatory (like IFNγ and TNFα) and anti-inflammatory (IL-10) cytokines, but the pathways and cells involved in this mechanisms are not clear yet [12]. It is a tetracosactide fact that not all microorganisms have the same effect on the host, and that probiotic properties are strain and host specific. In this sense, it is not possible to extrapolate the effects found with one probiotic strain to another, or its effect against a specific pathogen to other pathogen [13]. L. casei CRL 431 is a probiotic bacterium and its effects on the gut immune cells have been extensively studied. In a previous work, the effect of L. casei CRL 431 in the prevention of S. Typhimurium infection in BALB/c mice was evaluated. It was demonstrated that 7 days of L. casei CRL 431 administration before S. Typhimurium infection decreased its severity.