However, un-controlled inflammation is harmful to the host and eventually damages the niche involved Salmonella find protocol growth. AvrA plays a role opposite to that of the other known effectors by inhibiting the inflammatory responses in intestine. Hence, one could argue that AvrA’s role in inhibiting inflammation allows the pathogen to survive well in the host, thus establishing a mutually beneficial relationship. Our current study investigated gene expression at the mRNA level in response to AvrA. Posttranscriptional modification by AvrA cannot be identified by DNA array analysis. Study using Western blot and other protein assay methods will provide further insights into the AvrA’s regulation of eukaryotic proteins

in intestine. Taken together, our findings show that AvrA specifically inhibits inflammatory responses and promotes proliferation in vivo. It is important to understand how AvrA works in vivo because of the Salmonella problems and the bioweapon threat of bacterial toxins. We believe that studies on the action of bacterial effectors will uncover new facets

of bacterial-host interaction that may lead to the development of new therapeutic drugs or vaccines against important human pathogens. Acknowledgements We thank Dr. Constance D. Baldwin at the University of Rochester for critical revising and editing of this manuscript, Xi Emma Li for her excellent technical support, Julia Militar for helpful editing, and Jody Bown for helpful suggestion on microarray software. This work was supported by the NIDDK KO1 DK075386 and the American Cancer Trichostatin A Society RSG-09-075-01-MBC to Jun Sun. Electronic supplementary material Additional file 1: Table S1. Mirabegron Primer sequence for qRT-PCR. Listing all primer sequences used in qRT-PCR (PDF file). PCR data were shown in Figure 3. (PDF 238 KB) Additional file 2: Table S2. Differentially expressed genes between the SL1344 MK-8776 mouse infection and the SB1117 infection at early stage. The list of differentially expressed genes

between the SL1344 infection and the SB1117 infection at 8 hours post-infection (P ≤ 0.05 with fold change≥1.2 or ≤-1.2). (XLSX 50 KB) Additional file 3: Table S3. Differentially expressed genes between the SL1344 infection and the SB1117 infection at late stage. The list of differentially expressed genes between the SL1344 infection and the SB1117 infection at 4 days post-infection (P ≤ 0.05 with fold change≥1.2 or ≤-1.2). (XLS 102 KB) Additional file 4: Table S4. Target pathway of down-regulated genes in SL1344vs SB1117 infection group at 8 hours. Listing target pathway of down-regulated genes in SL1344vs SB1117 infection group at 8 hours post-infection. (PDF 252 KB) Additional file 5: Table S5. Target pathway of down-regulated genes in SL1344 vs SB1117 infection group at 4 days. Listing target pathway of down-regulated genes in SL1344vs SB1117 infection group at 4 day post-infection. (PDF 250 KB) References 1.