We also observed an increase in the microbicidal activity of alveolar macrophages of Lr1505- and Lc431-treated mice; this activity was significantly greater in the latter group (Table 1). Furthermore, the microbicidal activity of alveolar macrophages from the Lr1506-treated group was similar to that of the control mice. We next evaluated cytokine production by macrophages challenged in vitro with the pathogenic strain C. albicans selleck products AV4. All treatments increased production of TNF-α and IL-1β in peritoneal

macrophages; we observed no significant differences between treatments (Fig. 3a). Administration of Lr1505 and Lc431 increased the capacity of alveolar macrophages to produce TNF-α and IL-1β in response to C. albicans challenge, whereas administration of Lr1506 did not induce changes in the concentrations Roxadustat solubility dmso of these

cytokines (Fig. 3b). To evaluate the effect of lactobacilli treatments on peritoneal macrophages in vivo, we challenged the various groups of mice intraperitoneally with 108 cells of pathogenic C. albicans AV4 and took samples from liver, spleen and blood 48 hours later to analyze the presence of yeasts. Untreated control animals had positive counts of the pathogen in all the studied tissues (Table 2). Lc431, Lr1505 and Lr1506 treatments significantly reduced C. albicans counts in the liver during the studied period. In addition, animals treated with the different lactobacilli strains were able to eliminate the pathogenic yeast from blood and spleen (Table 2). In addition, in order to evaluate the influence

selleck inhibitor of Lc431, Lr1505 and Lr1506 on the activity of alveolar macrophages in vivo, we challenged the various groups of mice intranasally with 107 cells of pathogenic C. albicans AV4 and 48 hours later, took samples of lung and blood to determine the presence of yeast. The control animals had positive pathogen counts in both lung and blood (Table 2). Mice treated with Lc431 or Lr1505 had significantly lower C. albicans counts in the lungs than did the control group; Lr1506 did not induce changes in this variable. Moreover, all treatments were able to induce clearance of the pathogenic yeast from blood (Table 2). We next studied the immune response in the peritoneal cavity after challenge with C. albicans AV4. The number of leukocytes, macrophages and neutrophils in the peritoneal cavity increased in all experimental groups after challenge with the pathogen (Fig. 4a, b). However, mice treated prophylactically with Lc431, Lr1505 or Lr1506 had significantly greater macrophage and neutrophil counts than did those in the control group (Fig. 4a, b). We also observed increased concentrations of TNF-α and IFN-γ in peritoneal fluid after challenge with the pathogen in all experimental groups (Fig. 4c, d). However, groups receiving lactobacilli had greater cytokine concentrations than did controls. Nasal challenge with pathogenic C.