Figure 1 Hierarchical clustering analysis of 913 genes from Affymetrix array analysis showing differential expression patterns during SL1344 (WT AvrA) infection and SB1117(AvrA-) infection. Semaxanib supplier A indicates repressed gene cluster at 8 hours and 4 days; B indicates a up-expressed gene cluster at 8 hours but a down-expressed cluster at 4 days; C indicates a down-expressed gene cluster at 8 hours but a up-expressed cluster at 4 days; and D indicates an induced gene cluster at 8 hour and 4 days. Subset group was indicated with*. The heat map was built by using Gene Cluster 3.0 software. Red color represents up-regulation and green shows
down-regulation. We further identified some subset groups (indicated with *), which suggested that SL1344 and SB1117 infection differentially regulated genes at both the early stage and the late stage. These results indicate that AvrA is involved in altering host responses
in the Salmonella-intestine interaction in vivo. Characteristics of differentially expressed genes between the SL1344 and SB1117 infection groups Our cluster analysis CB-839 mw for the SL1344 (AvrA+) and SB1117 (AvrA-) infection groups have indicated that AvrA expression in the Screening Library manufacturer salmonella strains clearly alters the in vivo host responses to intestinal infection. In order to get a broad overview of the mouse colon transcriptional changes induced by Salmonella Typhimurium SL1344 effector AvrA, fold change in gene expression was calculated
for each SL1344 infection group relative to each SB1117 infection group (Figure 2). Figure 2 The number of differentially expressed genes between infection with salmonella, SL1344 (WT, AvrA) and SB1117(AvrA-). In the SL1344 infection group, compared to the SB1117 infection group, at 8 hours post infection, Edoxaban 347 (58%) genes were up-regulated and 227 genes (42%) were down-regulated (Figure 2 and Additional file 2 Table S2, Fold times ≥1.2 times, P ≤ 0.05). In the SL1344 infection group at 4 days, 268 genes (44%) in the group were up-regulated and 337 genes (56%) were down-regulated, compared to the SB1117 infection group (Figure 2 and Additional file 3 Table S3, Fold times ≥1.2 times, P ≤ 0.05). The majority of the genes that were differentially expressed between groups showed moderate alterations in expression of 1.2 to 2.0 folds (Additional file 2 Table S2 and Additional file 3 Table S3). Overall, the results indicate that AvrA protein by TTSS must be responsible for the induction and repression of in vivo transcriptional reprogramming of the host cells in intestinal infection (Figure 2).