1 and a fold change (FC) ≥ 1.5 were further analyzed. With IPA, the following functions were found to be significantly affected by dexamethasone (listed in the order of significance from highest to lowest): cell death,

small molecular biochemistry, immunological disease, cellular movement, cell-to-cell signaling and interaction, immune cell trafficking, antigen presentation, cell-mediated immune response, humoral immune response, inflammatory response, respiratory disease, cell signaling, infectious disease, organ injury and abnormality, and free radical selleck inhibitor scavenging. These functions were also affected by Pneumocystis infection, but in a different order of significance (also listed in the order of significance from highest to lowest): antigen presentation, cell-mediated immune response, humoral immune response, and inflammatory learn more response were equally and most severely affected, followed by cellular movement, immune cell trafficking, immunological disease, cell-to-cell signaling and interaction, cell death, organ injury and abnormality, cell signaling, infectious disease, small molecular biochemistry, antimicrobial response, and free radical scavenging (Fig. 3). Figure 3 Functions affected by dexamethasone or Pneumocystis infection. Cellular functions identified by IPA as being affected by dexamethasone or Pneumocystis infection are illustrated with

bar graphs based on the levels of -log(p-value), the higher the levels the more significant of the effect. Black bars indicate functions affected by dexamethasone treatment, while open bars denote those affected by Pneumocystis infection. The functions that were affected by Pneumocystis infection were further classified into four major groups: immune response, inflammation, cell death, and phagocytosis (Fig. 4). The immune response group included cell-mediated immune response, humoral immune response, and antigen presentation.

The cell death group included cell death and organ injury and abnormality; while cell signaling, cell-to-cell interaction, cell movement, anti-microbial response, immune cell trafficking, and free radical scavenging were included in the phagocytosis group. Genes that were differentially expressed due to Pneumocystis infection not dexamethasone treatment in each group are Fludarabine concentration shown in Table 1. It is interesting to note that these four functions share many of the same genes. Among these, Lgals1, Alcam, and Cd55 genes were down regulated; while Sod2, Soc3, Prf1, Il10, Mmp7, Sell, Psmb9, Oas1a, Clu, Ccr1, Mx1, Il8rb, Ccr5, Ccl5, Irf7, Nos2, and Cxcl10 genes were up regulated in all four functional groups. Cat and Hip1 genes that belong to both the cell death and phagocytosis groups were down regulated. In the cell death group, Hdac2, Bnip3L, Nr1h3, and Ppp6C genes were down regulated, and the Tap2 gene was up regulated.