Dexamethasone is well documented to interfere with the synthesis of IL-1b, an action thought to be at the transcriptional level of the IL-1 gene involving blocking NFKB and activator protein 1 activation with mRNA destabilization. Dexamethasone has been observed to decrease CCL2 expression in spiral ligament fibrocytes but has also been reported to be ineffective in human visceral adipose tissue suggesting that its effects are cell specific. In fact, there is evidence that the CCR2 participates in protection against noise-induced cell death and the expression of CCL2 is increased in this type of trauma. It is feasible that increased CCL2 expression provoked by both normal and dexamethasone-eluting electrodes constitutes a protective Wortmannin mechanism for the hair cells. Growth-regulated oncogene a, GROb, GROc are a family of proteins involved in modulating inflammatory responses. Three distinct GRO isoforms have been identified and now are referred to as CXCL1, CXCL2, and CXCL3 respectively. Insertion of the normal electrode into the guinea pig cochlea elevated expression, 2.7-fold, of GRO precursor with dexamethasone further increasing expression 4.3-fold. Previous studies have observed that dexamethasone both inhibits and increases CXCL1 expression. It is not clear why dexamethasone increases expression levels of the eotaxine and GRO precursor in the cochlea and this requires further elucidation. CD46, a regulator of complement activation, is expressed on all nucleated cells in humans, whereas CD150, a self-ligand co-stimulatory molecule, is expressed on thymocytes, activated lymphocytes, mature dendritic cells and macrophages, and nectin-4 is expressed on epithelial cells. It has been demonstrated that vaccine strains of MV use CD46 and CD150 for cellular entry while wild type strains use only CD150. The cellular distribution and expression of CD150 is consistent with the lymphotropism observed in wild type MV infections in vivo, whereas nectin-4 is used by the virus to leave an organism late in infection via the respiratory epithelium. A comparison of human CD150 with mouse CD150 demonstrated that the V region is crucial for binding to the MV hemagglutinin. Throughout history, morbillivirus infections have had an often devastating impact on both human and animal health. Phylogenetically, measles virus and rinderpest virus are the two most closely related morbilliviruses. In fact, RPV is thought to be the progenitor of MV which was passed on to humans by domesticated cattle and subsequently evolved into MV. It is also thought that RPV is the progenitor of canine distemper virus, a more distantly related morbillivirus of carnivores, and that the consumption of RPV infected prey led to the infection of carnivores and the evolution of CDV. An argument supporting this evolution is the common use of CD150 of the respective species as a cellular receptor for viral entry by these three morbilliviruses. In addition to using the species-specific respective CD150 molecules, MV, CDV and RPV can also use their non-species counterparts as receptors, although with reduced efficiency. In contrast, mouse CD150 does not support MV binding and entry and this might help to explain the lack of infection by MV in the mouse. The cotton rat replicates MV in its respiratory tract and lymphoid tissue after intranasal inoculation. As in humans, viral spread is restricted for vaccine virus in contrast to wild type virus. This difference in viral spread could be reproduced using two recombinant viruses which differed in their receptor usage in tissue culture versus CD150. These data indicated a dual receptor use and suggested that cotton rat CD150 might act as entry receptor.