The first cluster includes 8 genes up-regulated at t=+1 and related to immune cell tracking (ALOX12, JUNB, TNFAIP3, CCL20, CXCL5, NFKBIA, LTA, EDN1). Inflammation is a powerful protective mechanism which is coordinated and controlled by cytokines and chemokines and, as expected, we detected an increase in the expression level of members of the CXCL family. JUNB gene (a member of Jun family) also participates in the immune response; it is activated by the TLR signalling pathway  and can induce expression of interleukins [40–43]. Hormone activation of the glucocorticoid receptor in leukocytes results in a profound suppression of pro-inflammatory gene networks such as the NF- κB mediated transcription of pro-inflammatory cytokine genes and CXCL2 together with LTA were described by  as glucocorticoid-regulated genes. These findings show that wide variation in glucocorticoid sensitivity exists between individuals which may influence susceptibility to inflammatory diseases .