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. Author manuscript; available in PMC: 2016 Aug 17.
Published in final edited form as: Mucosal Immunol. 2016 Jan 27;9(5):1317–1329. doi: 10.1038/mi.2015.138

Figure 4.

Figure 4

PTP1B hinders S100A9 expression during RSV infection. Gene expression profiling of lung tissue from wild type and Ptp1b-deficient mice was performed 5 dpi. qPCR arrays were performed using the BioRad PrimePCR Apoptosis and Survival panel to examine over 350 genes associated with cell survival and apoptosis. (A) Data were analyzed with the BioRad PrimePCR analysis software. Color code in the clustergram shows standardized gene expression responses from the microarray probes of samples from RSV infected wild type and Ptp1b-/- mice. Red indicates higher expression and green lower expression. (B) Expression values were log2 transformed and normalized to compare wild type and Ptp1b-/- gene expression. Threshold lines demonstrate significantly greater differences in expression between both groups. S100A9, a gene negatively regulated by PTP1B, was examined in the (C) BALF and (D) lung tissue of wild type and Ptp1b-/- mice. (D) Tissue was stained for RSV antigen (red) and fluorescent intensity quantified. S100A9 immunoblots were also conducted on lung tissue. (E) Gene expression of S100A9 is inducible in human SAE cells and murine BMDM following RSV infection. (F) Stimulus of S100A9 protein induces release of MCP-1, PDGF, CXCL10, CXCL1 and CXCL9 from SAE human cells transfected with negative/scrambled (Scr.) or PTP1B siRNA. Graphs are represented as mean ± S.E.M, where n=10 per group. qPCR is represented as relative quantification (RQ). (C) * p < 0.05 compared to wild-type mice on each corresponding time point. (E-F) p values shown, comparing both treatments connected by a line.