Results & discussion MAP concentrations in intestinal and liver tissues Data described in Table 1 and Figure 1 and TH-302 manufacturer Figure 2 reveal that MAP cells were present in intestinal tissues and the liver- Buparlisib nmr organs which are associated with MAP infection and pathogenesis. Additionally, these data demonstrate that regardless of NP-51 consumption viable MAP cells were able to invade host tissues- as evidenced by granuloma formation in liver samples of animals fed viable or non-viable NP-51. However,

lower concentrations of MAP cells were observed in both intestinal and liver tissues at Day 90 (45 days post MAP infection) in animals that were also fed viable or nonviable NP-51, although not significant. There were no significant changes in MAP concentrations from intestinal tissues and an increase in learn more liver MAP concentrations were observed from Day 90 through Day 180, suggesting that MAP viability may not be deterred through the presence of probiotics (see Figure

1 and Figure 2). Table 1 Total animals (n = 4) demonstrating granuloma formations in liver tissues   K-MAP K-MAP + L-NP-51 L-MAP L-MAP + L-NP-51 Day 90 3/4 3/4 4/4 4/4 Day 135 2/2* 3/4 4/4 3/4 Day 180 3/4 2/4 2/4 3/4 Tissues were stained with Hemotoxylin & Eosin (H & E stain) prior to evaluation. For K-MAP samples at Day 135, only two sets of animal tissues were available for examination due to early expiration of animals before the harvest date (these data are highlighted with ‘*’). Control animals did not demonstrate granuloma formation at Day 90 and Day 180; Day 135 control animals

were contaminated and were positive for granulomas in liver tissues. The data represent the number of animals that demonstrated granuloma formations per total animals examined (n =4). Experimental eltoprazine groups included are the following: animals fed normal chow and infected with viable MAP cells (Live-MAP; L-MAP); animals fed viable probiotics in chow and uninfected (Live NP-51; L-NP-51); animals fed viable probiotics in chow and infected with non-viable MAP cells (K-MAP + L-NP-51); animals fed viable probiotics in chow and infected with viable MAP cells (L-MAP + L-NP-51). These data demonstrate MAP infection of tissues regardless of viable or non-viable NP-51 consumption. Additionally, these data evidence that host tissues produce granulomas from exposure to K-MAP antigens. Figure 1 qRT-PCR Assay to Quantitate MAP from Infected BALB/c Mouse Tissues. Concentrations were determined using qRT-PCR analysis from large intestine and liver; The experimental groups analyzed were the following: Control (CNTRL); viable MAP (MAP); viable MAP with non-viable (killed) NP-51 (MAP + K-NP-51); viable MAP with viable (live) NP-51 (MAP + L-NP-51). For each experimental group n = 4. A: MAP Concentration in Large Intestinal Tissues. At DAY 180- there was a significant difference ‘*’ (P ≤ 0.