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Listeria monocytogenes is a foodborne pathogen causative of opportunistic infections. Listeriosis is associated with severe infections in pregnant women causing abortion or neonatal listeriosis. An alternative to antibiotics are safe novel bacteriocins peptides such as enterocin CRL35 with strong antilisterial activity produced by Enterococcus mundtii CRL35. In the present paper, our goal is to study the effectiveness of this peptide and the producer strain in a murine model of pregnancy-associated listeriosis. A single dose of 5×10(9) colony-forming unit of L. monocytogenes FBUNT (Faculty of Biochemistry-University of Tucumán) resulted in translocation of pathogen to liver and spleen of BALB/c pregnant mice. The maximum level of Listeria was observed on day 3 postinfection. Interestingly, the intragastric administration of enterocin CRL35 significantly reduced the translocation of the pathogen to vital organs. On the other hand, the preadministration of E. mundtii CRL35 slightly inhibited this translocation. Listeria infection caused a significant increase in polymorphonuclear leukocytes at day 3 postinfection compared to the noninfected group. This value was reduced after the administration of enterocin CRL35. No significant changes were observed in either white blood cells or lymphocytes counts. Based on the data presented in the present work enterocin CRL35 would be a promising alternative for the prevention of Listeria infections.

Background: We have previously demonstrated that Lactobacillus casei CRL 431 administration improved the resistance to pneumococcal infection in a mouse model.

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Streptococcus pneumoniae is able to activate coagulation and induce platelet aggregation, both of which are typical responses to systemic inflammation. The interactions between inflammation and coagulation and between soluble adhesion molecules and endothelial cells are important in the pathogenesis of an unbalanced haemostatic system. Therefore, an exaggerated and/or insufficiently controlled haemostatic activity may appreciably contribute to the severity of the disease. The aim of the present study was to evaluate the effect of the oral administration of Lactobacillus casei CRL 431 on platelet and endothelial activation mechanisms in a respiratory pneumococcal infection model in mice. S. pneumoniae induced an increase in platelet counts and enhanced the expression of P-selectin in control group, with higher endothelial activation in lung shown by the increase in von Willebrand factor (vWF) and vascular cell adhesion molecule 1 (VCAM-1) expression. Also, infection induced a decrease in CXCR-4 leukocytes, increased expression in annexinV and cell death at the pulmonary level and decreased antithrombin levels in bronchoalveolar lavage. In contrast, L. casei mice restored platelet counts, favoured faster P-selectin expression, lower vWF levels and VCAM-1 expression than control group. Also, L. casei induced higher levels of annexinV expression and lower cell death in the lung. Moreover, it was able to modulate antithrombin levels within the normal range, which would indicate lower coagulation activation and a protective effect locally exerted by L. casei. In this work, the ability of L. casei to favourably modulate platelet and endothelial functionality during a pulmonary infection with S. pneumoniae was demonstrated. Our findings offer a promising perspective for the use of this probiotic strain in the prevention of thrombotic complications associated with pneumococcal pneumonia, especially in at-risk patients. In addition, the use of L. casei would provide novel alternatives for the prevention and treatment of thrombosis associated with various diseases.