Clostridium butyricum Ameliorates Salmonella Enteritis Induced Inflammation by Enhancing and Improving Immunity of the Intestinal Epithelial Barrier at the Intestinal Mucosal Level

To estimate the global burden of nontyphoidal Salmonella gastroenteritis, we synthesized existing data from laboratory-based surveillance and special studies, with a hierarchical preference to (1) prospective population-based studies, (2) "multiplier studies," (3) disease notifications, (4) returning traveler data, and (5) extrapolation. We applied incidence estimates to population projections for the 21 Global Burden of Disease regions to calculate regional numbers of cases, which were summed to provide a global number of cases. Uncertainty calculations were performed using Monte Carlo simulation. We estimated that 93.8 million cases (5th to 95th percentile, 61.8-131.6 million) of gastroenteritis due to Salmonella species occur globally each year, with 155,000 deaths (5th to 95th percentile, 39,000-303,000 deaths). Of these, we estimated 80.3 million cases were foodborne. Salmonella infection represents a considerable burden in both developing and developed countries. Efforts to reduce transmission of salmonellae by food and other routes must be implemented on a global scale.

Salmonella species cause substantial morbidity, mortality and burden of disease globally. Infections with Salmonella species cause multiple clinical syndromes. Central to the pathophysiology of all human salmonelloses is the induction of a strong host innate immune/inflammatory response. Whether this ultimately reflects an adaptive advantage to the host or pathogen is not clear. However, it is evident that both the host and pathogen have evolved mechanisms of triggering host responses that are detrimental to the other. In this review, we explore some of the host and pathogenic mechanisms mobilized in the two predominant clinical syndromes associated with infection with Salmonella enterica species: enterocolitis and typhoid.

Four hundred and fifty 1-d-old male Lingnan Yellow broiler chickens were used to investigate the effects of Clostridium butyricum on growth performance, immune function, and cecal microflora. The birds were randomly assigned to 5 treatments and offered the same antibiotic-free basal diets for 42 d. The treatments were as follows: no addition (control), 1 × 10(7) cfu C. butyricum/kg of diet (CB1), 2 × 10(7) cfu C. butyricum/kg of diet (CB2), 3 × 10(7) cfu C. butyricum/kg of diet (CB3), and 10 mg of colistine sulfate/kg of diet (antibiotic). Birds fed either CB2 or antibiotic had greater overall BW than those in the control group. During d 1 to 7, d 21 to 42, and d 1 to 42, birds fed either CB2 or CB3 or the antibiotic diet had greater ADG compared with those in the control group. No significant differences were observed in BW or ADG among the CB2, CB3, and antibiotic groups. Birds fed the CB2 or CB3 diet had greater concentrations of IgA and IgG in the serum from d 14 to 42 and greater IgM in the serum from d 21 to 42 than those in the control group. Birds fed the CB3 diet had a greater concentration of complement component 3 in the serum than those in the control group from d 7 to 42. Dietary C. butyricum decreased (P < 0.05) Escherichia coli in cecal contents on d 14 and 42, and both CB2 and CB3 decreased (P < 0.05) cecal Salmonella and Clostridium perfringen from d 14 to 42 compared with the control. Broilers fed either CB2 or CB3 had greater cecal Lactobacillus and Bifidobacterium counts from d 21 to 42, and birds fed C. butyricum had greater cecal C. butyricum counts during the whole period compared with those in the control group. The results indicate that C. butyricum promotes growth performance and immune function and benefits the balance of the intestinal microflora in broiler chickens.