IL1B and Arthritis: The induction and maintenance of joint pain are associated with intense CXCL1-mediated neutrophil influx and production of hyperalgesic mediators, such as IL-1β (Cunha et al., 2010; Sachs et al., 2011; Amaral et al., 2012), and blockade these mediators have been described to suppressed joint pain and damage in murine model of arthritis (Williams et al., 2000).