However, IL-8 was found in all intestinal samples from the pigs infected with Salmonella. The flagellin of this bacterial species is its main inducer [44]. As a flagellated bacterium, EcN also induces IL-8 in enterocytes [45,46] and this could be one of the mechanisms by which it protects against Salmonella infection [25,43]. High plasma levels of IL-10 were observed in piglets infected with Salmonella alone or in piglets colonized with bifidobacteria and infected with Salmonella. IL-10 levels Erlotinib solubility dmso correlated with TNF-α levels and with the presence of Salmonella in blood, suggesting an interplay between both cytokines,

or more generally the interplay between pro- and anti-inflammatory reactions. In contrast, IL-10 was absent in the blood of piglets colonized with EcN and subsequently infected with Salmonella. Blood IL-10 levels increase in several septic states, including E. coli sepsis [47] and a swine model of shock caused by heat-killed Neisseria meningitis[48]. The continued presence of IL-10 in blood 24 h after infection of gnotobiotic pigs with S. Typhimurium seems to be a prognostic marker of poor survival in infected animals [43]. Levels of IL-10 also reflect the severity of Salmonella infection in mice [49]. In contrast, increased levels of IL-10 in blood coincided with recovery from experimentally induced swine dysentery [50]. In this study, IL-10 was not

found in any intestinal sample. This may be caused by the absence of cells capable of producing it, e.g. by the paucity and immaturity of T lymphocytes in intestinal villi of germ-free pigs. High levels of TNF-α were found in plasma and ileum of piglets infected click here with Salmonella alone or in Atezolizumab mouse piglets pre-colonized with bifidobacteria before this infection. The statistically significant reduction in TNF-α in pigs di-associated with EcN and LT2 correlated with the ability of EcN to interfere with Salmonella in the ileum and ultimately stop translocation to the mesenteric lymph nodes.

The levels of TNF-α are markers of inflammation and high levels are found in bacteraemia. Rapid turnover of TNF-α in blood of pigs challenged by living or heat-killed bacteria or bacterial lipopolysaccharide has been described [47,48]. Prolonged presence of TNF-α in blood circulation was seen in our experimental gnotobiotic piglets which, together with IL-10 levels, correlated with increased lethality. Decreasing levels or neutralization of TNF-α in blood can be one method of protection against the lethal sequelae of bacteraemia [51]. Preliminary association of germ-free piglets with EcN significantly reduced levels of TNF-α in Salmonella-infected piglets compared to animals infected with Salmonella alone. Unlike conventional animals, the germ-free animals show no resistance to colonization [3], and a single dose of bacteria suffices for the prolonged colonization of their gastrointestinal tract.