Upregulation of CXCL1/CXCR2 signaling is central to neuroinflammation following exposure to bacterial endotoxin, (Kielian et al., 2001; Carlson et al., 2008; Kerstetter et al., 2009; Liu et al., 2010; Roy et al., 2012) and CXCL1 is rapidly upregulated in traumatic brain injury (TBI), Alzheimer’s disease, multiple sclerosis, chronic pain and stroke, and is followed by neural cell specific increases in CXCR2 expression (Valles et al., 2006; Lindner et al., 2008; Kerstetter et al., 2009; Liu et al., 2010, 2015; Cao et al., 2014; Connell et al., 2015; Ryu et al., 2015). Here, CXCR2 is linked to early-onset autosomal dominant Alzheimer disease.