Because PR/8 infection increased secretion of TNF-a and increased gene expression of IL-1 family members, well-known proinflammatory mediators that cause release of inflammatory chemokines, we were interested in the impact of these proinflammatory mediators on the overall chemokine response during the infection in human AM. Our hypothesis was that TNF and IL-1 signaling would augment chemokine secretion in a paracrine manner [29] . As shown in Figure 5 , neutralization of TNF pathway by its soluble receptor significantly decreased secretion of CXCL8 by 65% (P,0.001) and CCL5 by 53% (P,0.05), but did not alter secretion of IFNs, CXCL10, or TNF-a itself. Blockade of the IL-1 receptor by its naturally occurring receptor antagonist IL-1Ra [30] had a similar effect. When the activity of both cytokines was inhibited, there was no further reduction in chemokines greater than that of a single inhibitor, although there was a slight decrease in CXCL10 response in the presence of both inhibitors, the response was not statistically significant.