While the inhibition of proinflammatory interleukins (e.g., IL17C, IL17F and IL8) and CXC chemokines (e.g., CXCL12b and CXCL19) could be a mechanism to prevent an excessive inflammatory response that could potentially harm the host’s own cells (62), it might rather indicate a suppression of the host defense mechanisms induced by T. maritimum secretory/excretory products, rendering fish more vulnerable to infection (33, 67). This evidence concerns the gene CXCL8 and infection.